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University of Manchester
1.
Abdalla, Zahra.
Investigation of E-cadherin expression in oral epithelial
dysplasia and squamous cell carcinoma.
Degree: 2016, University of Manchester
URL: http://www.manchester.ac.uk/escholar/uk-ac-man-scw:299283 
► Oral squamous cell carcinoma (OSCC) is a highly aggressive cancer that is characterized by a high rate of invasion and destruction to the surrounding tissues,…
(more)
▼ Oral squamous cell carcinoma (OSCC) is a highly
aggressive cancer that is characterized by a high rate of invasion
and destruction to the surrounding tissues, with patients showing
poor 5-year survival rate. A pre-malignant stage of cellular atypia
and loss of stratification within the epithelium (dysplasia) occurs
prior to the establishment of OSCC, which is manifested as white
(leukoplakia) or red (erythroplakia) lesions. Treatment of
dysplasia/OSCC involves surgical intervention with the removal of
an adequate safety margin. However, high grade dysplasia and OSCC
exhibit high recurrence rates. To date the only method used to
diagnose oral epithelial dysplasia (OED) and OSCC is haematoxylin
and eosin staining of biopsies and examination by an experienced
pathologist. Furthermore, the mechanisms of dysplasia formation,
transition to OSCC, and high recurrence rates are little
understood. Recent data from the Ward lab suggests that the cell
surface tumour suppressor protein
E-
cadherin plays an important
role in regulating many cellular functions in epithelial cells.
Loss of
E-
cadherin in carcinomas has been well studied and is
linked with tumour invasion, metastasis and poorer patient
outcomes. In this thesis, I have investigated expression of
E-
cadherin in low grade (LG) and high grade (HG) dysplasia and T1
and T4 OSCC patient biopsies to determine whether loss of this
protein occurs prior to tumour cell invasion. Furthermore,
microarray data analysis identified Epithelial Membrane Protein-1
(EMP-1) as a putative early marker of tumorigenesis, with
alterations of N-
cadherin, CD44 and 5T4 oncofoetal antigen
expression during tumorigenesis inferred from our studies in
embryonic stem cells. Immunofluorescence microscopy (IFM) analysis
revealed that normal oral epithelium exhibits cell surface
E-
cadherin, EMP-1 and 5T4 expression but generally lacks N-
cadherin
and CD44 reactivity. The statistically significant loss of both
E-
cadherin and EMP-1 was observed in low and high grade dysplastic
tissue and OSCC biopsies (p<0.001). 5T4 expression was decreased
in HG dysplasia (p<0.001), suggesting this may be a useful assay
for discriminating between LG and HG dysplastic tissues. N-
cadherin
or CD44 did not show any statistical significance in expression
between normal, LG/HG dysplasia and T1/T4 OSCC, although there was
a trend for increased N-
cadherin expression in T4 OSCC.
Significantly,
E-
cadherin expression was decreased or absent from
surgical margins of LG/HG dysplasia and T1 OSCC, and EMP-1 and 5T4
were absent from the margins of LG and HG dysplastic tissue,
indicating that these margins are abnormal. Therefore, loss of
E-
cadherin and EMP-1 are early events associated with dysplastic
tissue and may be a useful method to confirm the removal of
sufficient surgical safety margin. The OSCC cell line BICR56 was
assessed for marker expression and exhibited a phenotype consistent
with normal oral epithelium. Inhibition of
E-
cadherin protein in
BICR56 cells using a neutralising antibody led to decreased cell
surface localisation…
Advisors/Committee Members: MERRY, CATHERINE CLR, Merry, Catherine, Ward, Christopher.
Subjects/Keywords: E-cadherin; OSCC
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APA (6th Edition):
Abdalla, Z. (2016). Investigation of E-cadherin expression in oral epithelial
dysplasia and squamous cell carcinoma. (Doctoral Dissertation). University of Manchester. Retrieved from http://www.manchester.ac.uk/escholar/uk-ac-man-scw:299283
Chicago Manual of Style (16th Edition):
Abdalla, Zahra. “Investigation of E-cadherin expression in oral epithelial
dysplasia and squamous cell carcinoma.” 2016. Doctoral Dissertation, University of Manchester. Accessed January 19, 2021.
http://www.manchester.ac.uk/escholar/uk-ac-man-scw:299283.
MLA Handbook (7th Edition):
Abdalla, Zahra. “Investigation of E-cadherin expression in oral epithelial
dysplasia and squamous cell carcinoma.” 2016. Web. 19 Jan 2021.
Vancouver:
Abdalla Z. Investigation of E-cadherin expression in oral epithelial
dysplasia and squamous cell carcinoma. [Internet] [Doctoral dissertation]. University of Manchester; 2016. [cited 2021 Jan 19].
Available from: http://www.manchester.ac.uk/escholar/uk-ac-man-scw:299283.
Council of Science Editors:
Abdalla Z. Investigation of E-cadherin expression in oral epithelial
dysplasia and squamous cell carcinoma. [Doctoral Dissertation]. University of Manchester; 2016. Available from: http://www.manchester.ac.uk/escholar/uk-ac-man-scw:299283
University of Otago
2.
D'Costa, Zarina.
Regulation of E-cadherin by Human Papillomavirus type 16 E6
.
Degree: 2011, University of Otago
URL: http://hdl.handle.net/10523/1903
► The primary risk factor for the development of cervical cancer is a persistent infection with certain high-risk human papillomavirus (HPV) types such as 16 and…
(more)
▼ The primary risk factor for the development of cervical cancer is a persistent infection with certain high-risk human papillomavirus (HPV) types such as 16 and 18. The ability of these viruses to cause such persistent infections within the host can be attributed to several immune evasion mechanisms. One such mechanism involves adversely affecting the amount of viral antigen presented to the host immune system. It was previously shown that the E6 oncoprotein of HPV16 is capable of actively down-regulating expression of epithelial (
E)-
cadherin expression which directly correlates with depletion in the number of immune Langerhans cells (LCs) in the infected tissue. In this manner, HPV16 E6 is able to contribute to viral survival and protection.
The aims of this study were firstly, to investigate the mechanism of E6 regulation of
E-
cadherin; secondly, to identify a region of E6 responsible for regulation of
E-
cadherin; thirdly, to investigate the roles of the other HPV16 oncoproteins in
E-
cadherin regulation and fourthly, to identify potential therapeutic interventions for early HPV16 infections.
The E6 oncoprotein from HPV16 was expressed in HCT116 cells and its ability to regulate
E-
cadherin promoter, transcript and surface protein was investigated. E6 was found to regulate
E-
cadherin at a transcriptional level. The
E-
cadherin promoter was found to be repressed in HCT116 E6 cells through a methylation dependent mechanism that is independent of direct methylation of the
E-
cadherin promoter. In order to identify the region of E6 oncoprotein important for
E-
cadherin regulation, a range of HPV16 E6 mutants were tested for their abilities to decrease transcription of
E-
cadherin. Mutational analysis of HPV16 E6 led to the identification of residues 118-122 and the nearby R124 residue, located within the C-terminal zinc-finger binding domain to be important for transcriptional regulation of
E-
cadherin by E6. In addition, the other major oncoproteins of HPV16, namely E5 and E7 were co-expressed with E6 and their abilities to regulate surface
E-
cadherin were assessed. E7 was also found to be effective in decreasing surface
E-
cadherin levels, and this effect was enhanced when the two oncoproteins were co-expressed in HCT116 cells. Furthermore, regulation of
E-
cadherin by HPV16 oncoproteins was assessed under conditions of differentiation using a simple monolayer model of differentiation and a three-dimensional organotypic raft culture system. Lastly, in order to identify potential therapeutic interventions for early HPV16 infections, rational design was used to design peptide antagonists of E6 that could potentially interfere with E6 regulation of
E-
cadherin. Despite efficient delivery of peptide inhibitors of E6 into target E6 expressing cells, no restoration of
E-
cadherin levels were detected. However, another potential therapeutic compound, Indole-3-carbinol, was identified.
This research gives insight into the mechanism of transcriptional regulation of
E-
cadherin by HPV16 E6. The data presented here suggest that…
Advisors/Committee Members: Hibma, Merilyn (advisor).
Subjects/Keywords: Human papillomavirus;
E-cadherin
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APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
D'Costa, Z. (2011). Regulation of E-cadherin by Human Papillomavirus type 16 E6
. (Doctoral Dissertation). University of Otago. Retrieved from http://hdl.handle.net/10523/1903
Chicago Manual of Style (16th Edition):
D'Costa, Zarina. “Regulation of E-cadherin by Human Papillomavirus type 16 E6
.” 2011. Doctoral Dissertation, University of Otago. Accessed January 19, 2021.
http://hdl.handle.net/10523/1903.
MLA Handbook (7th Edition):
D'Costa, Zarina. “Regulation of E-cadherin by Human Papillomavirus type 16 E6
.” 2011. Web. 19 Jan 2021.
Vancouver:
D'Costa Z. Regulation of E-cadherin by Human Papillomavirus type 16 E6
. [Internet] [Doctoral dissertation]. University of Otago; 2011. [cited 2021 Jan 19].
Available from: http://hdl.handle.net/10523/1903.
Council of Science Editors:
D'Costa Z. Regulation of E-cadherin by Human Papillomavirus type 16 E6
. [Doctoral Dissertation]. University of Otago; 2011. Available from: http://hdl.handle.net/10523/1903
University of Manchester
3.
Abdalla, Zahra Youssef.
Investigation of E-cadherin expression in oral epithelial dysplasia and squamous cell carcinoma.
Degree: PhD, 2016, University of Manchester
URL: https://www.research.manchester.ac.uk/portal/en/theses/investigation-of-ecadherin-expression-in-oral-epithelial-dysplasia-and-squamous-cell-carcinoma(8ad27ead-06f2-48e0-9a84-2ca12ea47f53).html
;
https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.740279
► Oral squamous cell carcinoma (OSCC) is a highly aggressive cancer that is characterized by a high rate of invasion and destruction to the surrounding tissues,…
(more)
▼ Oral squamous cell carcinoma (OSCC) is a highly aggressive cancer that is characterized by a high rate of invasion and destruction to the surrounding tissues, with patients showing poor 5-year survival rate. A pre-malignant stage of cellular atypia and loss of stratification within the epithelium (dysplasia) occurs prior to the establishment of OSCC, which is manifested as white (leukoplakia) or red (erythroplakia) lesions. Treatment of dysplasia/OSCC involves surgical intervention with the removal of an adequate safety margin. However, high grade dysplasia and OSCC exhibit high recurrence rates. To date the only method used to diagnose oral epithelial dysplasia (OED) and OSCC is haematoxylin and eosin staining of biopsies and examination by an experienced pathologist. Furthermore, the mechanisms of dysplasia formation, transition to OSCC, and high recurrence rates are little understood. Recent data from the Ward lab suggests that the cell surface tumour suppressor protein E-cadherin plays an important role in regulating many cellular functions in epithelial cells. Loss of E-cadherin in carcinomas has been well studied and is linked with tumour invasion, metastasis and poorer patient outcomes. In this thesis, I have investigated expression of E-cadherin in low grade (LG) and high grade (HG) dysplasia and T1 and T4 OSCC patient biopsies to determine whether loss of this protein occurs prior to tumour cell invasion. Furthermore, microarray data analysis identified Epithelial Membrane Protein-1 (EMP-1) as a putative early marker of tumorigenesis, with alterations of N-cadherin, CD44 and 5T4 oncofoetal antigen expression during tumorigenesis inferred from our studies in embryonic stem cells. Immunofluorescence microscopy (IFM) analysis revealed that normal oral epithelium exhibits cell surface E-cadherin, EMP-1 and 5T4 expression but generally lacks N-cadherin and CD44 reactivity. The statistically significant loss of both E-cadherin and EMP-1 was observed in low and high grade dysplastic tissue and OSCC biopsies (p < 0.001). 5T4 expression was decreased in HG dysplasia (p < 0.001), suggesting this may be a useful assay for discriminating between LG and HG dysplastic tissues. N-cadherin or CD44 did not show any statistical significance in expression between normal, LG/HG dysplasia and T1/T4 OSCC, although there was a trend for increased N-cadherin expression in T4 OSCC. Significantly, Ecadherin expression was decreased or absent from surgical margins of LG/HG dysplasia and T1 OSCC, and EMP-1 and 5T4 were absent from the margins of LG and HG dysplastic tissue, indicating that these margins are abnormal. Therefore, loss of Ecadherin and EMP-1 are early events associated with dysplastic tissue and may be a useful method to confirm the removal of sufficient surgical safety margin. The OSCC cell line BICR56 was assessed for marker expression and exhibited a phenotype consistent with normal oral epithelium. Inhibition of E-cadherin protein in BICR56 cells using a neutralising antibody led to decreased cell surface localisation…
Subjects/Keywords: 616.99; E-cadherin; OSCC
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APA ·
Chicago ·
MLA ·
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CSE |
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Manager
APA (6th Edition):
Abdalla, Z. Y. (2016). Investigation of E-cadherin expression in oral epithelial dysplasia and squamous cell carcinoma. (Doctoral Dissertation). University of Manchester. Retrieved from https://www.research.manchester.ac.uk/portal/en/theses/investigation-of-ecadherin-expression-in-oral-epithelial-dysplasia-and-squamous-cell-carcinoma(8ad27ead-06f2-48e0-9a84-2ca12ea47f53).html ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.740279
Chicago Manual of Style (16th Edition):
Abdalla, Zahra Youssef. “Investigation of E-cadherin expression in oral epithelial dysplasia and squamous cell carcinoma.” 2016. Doctoral Dissertation, University of Manchester. Accessed January 19, 2021.
https://www.research.manchester.ac.uk/portal/en/theses/investigation-of-ecadherin-expression-in-oral-epithelial-dysplasia-and-squamous-cell-carcinoma(8ad27ead-06f2-48e0-9a84-2ca12ea47f53).html ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.740279.
MLA Handbook (7th Edition):
Abdalla, Zahra Youssef. “Investigation of E-cadherin expression in oral epithelial dysplasia and squamous cell carcinoma.” 2016. Web. 19 Jan 2021.
Vancouver:
Abdalla ZY. Investigation of E-cadherin expression in oral epithelial dysplasia and squamous cell carcinoma. [Internet] [Doctoral dissertation]. University of Manchester; 2016. [cited 2021 Jan 19].
Available from: https://www.research.manchester.ac.uk/portal/en/theses/investigation-of-ecadherin-expression-in-oral-epithelial-dysplasia-and-squamous-cell-carcinoma(8ad27ead-06f2-48e0-9a84-2ca12ea47f53).html ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.740279.
Council of Science Editors:
Abdalla ZY. Investigation of E-cadherin expression in oral epithelial dysplasia and squamous cell carcinoma. [Doctoral Dissertation]. University of Manchester; 2016. Available from: https://www.research.manchester.ac.uk/portal/en/theses/investigation-of-ecadherin-expression-in-oral-epithelial-dysplasia-and-squamous-cell-carcinoma(8ad27ead-06f2-48e0-9a84-2ca12ea47f53).html ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.740279
Universiteit Utrecht
4.
Pilzecker, B.
The E- and N-cadherin switch in Epithelial to Mesenchymal Transition and metastasis.
Potential drug targets?.
Degree: 2013, Universiteit Utrecht
URL: http://dspace.library.uu.nl:8080/handle/1874/287101
► Carcinomas are most prevalent type of cancers and arise from an epithelial layer. Epithelial layers have a strict organization; cells are tightly linked through different…
(more)
▼ Carcinomas are most prevalent type of cancers and arise from an epithelial layer. Epithelial layers have a strict organization; cells are tightly linked through different junctions. The Epithelial to Mesenchymal Transition (EMT) developmental program enables epithelial cells to transform into mesenchymal cells and break free from neighboring epithelial cells in order to migrate though the body. Also in carcinomas, EMT enables cells to invade into healthy tissue. EMT also aids cancer progression in other manners by suppressing senescence, anoikis, apoptosis, oncogene addiction and modulating the immune response. Furthermore, EMT can lead to the formation of mesenchymal cancer stem cells. Mesenchymal cancer stem cells seem to be more resistant to chemotherapy than epithelial cancer cells. All of these traits increase the chance of an invading cancer cell being successful in setting up a metastatic niche. The
cadherin switch from
E-
cadherin to N-
cadherin is considered a mark of EMT. Cadherins are cell-cell adhesion proteins.
E-
cadherin inhibits invasion by protecting epithelial integrity and N-
cadherin increases invasion. It seems that a part of carcinomas has an
E- to N-
cadherin switch during EMT. However, other carcinomas show other
cadherin switches and
E- and N-
cadherin expression is not always mutually exclusive. In the HMLE cancer cell line
E-
cadherin knockdown is enough to induce EMT. By knocking out
E-
cadherin and p53 in a tissue specific manner they show an increase of invasion and metastases. In gastric carcinoma model
E-
cadherin and p53 knockout leads to EMT, however, in an invasive lobular carcinoma model EMT has not been observed. If EMT could be inhibited in carcinomas, the chance of metastasis would decrease and the formation of new cancer stem cells would be inhibited. Since chemotherapy mainly targets epithelial cancer cells, combining an EMT inhibitor might lead to more efficient chemotherapy. There are some compounds capable of inhibiting EMT or promoting the reverse process Mesenchymal to Epithelial Transition (MET). The identified compounds either inhibit a pathway which induces EMT or lead regaining epithelial identity and re-expression of
E-
cadherin. These compounds need to be further tested using in vivo models. Antibodies targeting mesenchymal marker proteins are being developed as well. An anti N-
cadherin antibody shows a decrease of tumor growth and metastases in mice, perhaps by targeting mesenchymal cancer stem cells. Since chemotherapy does not efficiently target cancer stem cells, screens were performed to find compounds that target cancer stem cells. In the future, there may be a combined anticancer therapy developed which inhibits EMT and targets cancer stem cells. This type of therapy could be combined with chemo-, radiotherapy or surgery to treat carcinomas more efficiently.
Advisors/Committee Members: Bos, Prof. Dr. J.L..
Subjects/Keywords: Carcinomas; Epithelial to Mesenchymal Transition (EMT); E-cadherin; N-cadherin
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APA ·
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MLA ·
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CSE |
Export
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Manager
APA (6th Edition):
Pilzecker, B. (2013). The E- and N-cadherin switch in Epithelial to Mesenchymal Transition and metastasis.
Potential drug targets?. (Masters Thesis). Universiteit Utrecht. Retrieved from http://dspace.library.uu.nl:8080/handle/1874/287101
Chicago Manual of Style (16th Edition):
Pilzecker, B. “The E- and N-cadherin switch in Epithelial to Mesenchymal Transition and metastasis.
Potential drug targets?.” 2013. Masters Thesis, Universiteit Utrecht. Accessed January 19, 2021.
http://dspace.library.uu.nl:8080/handle/1874/287101.
MLA Handbook (7th Edition):
Pilzecker, B. “The E- and N-cadherin switch in Epithelial to Mesenchymal Transition and metastasis.
Potential drug targets?.” 2013. Web. 19 Jan 2021.
Vancouver:
Pilzecker B. The E- and N-cadherin switch in Epithelial to Mesenchymal Transition and metastasis.
Potential drug targets?. [Internet] [Masters thesis]. Universiteit Utrecht; 2013. [cited 2021 Jan 19].
Available from: http://dspace.library.uu.nl:8080/handle/1874/287101.
Council of Science Editors:
Pilzecker B. The E- and N-cadherin switch in Epithelial to Mesenchymal Transition and metastasis.
Potential drug targets?. [Masters Thesis]. Universiteit Utrecht; 2013. Available from: http://dspace.library.uu.nl:8080/handle/1874/287101
5.
Nore, Andrea Marie.
Regulation Of Vectorial Active Transport In Human Proximal Tubule Cells By MT-3: The Role Of The C-Terminal Domain On E-And N-Cadherin Expression And The Confirmation Of Protein-Protein Interactions.
Degree: PhD, Biomedical Sciences, 2015, University of North Dakota
URL: https://commons.und.edu/theses/1938
► The proximal tubule of the kidney is particularly susceptible to toxicant-induced damage and cell cultures of human proximal tubule cells are widely utilized to…
(more)
▼ The proximal tubule of the kidney is particularly susceptible to toxicant-induced damage and cell cultures of human proximal tubule cells are widely utilized to study the role of epithelial-mesenchymal transition (EMT) in renal disease. Cadmium is a toxic metal ion that is known to produce renal tubular necrosis and accumulate in the proximal tubule. This metal binds to a family of cysteine rich metal binding proteins known as metallothioneins (MT) that are found in abundance in the kidney. Previous studies from our laboratory have shown that the third isoform of metallothionein (MT-3) is expressed in the epithelial cells of the human kidney, including those of the proximal tubule. An immortalized proximal tubule cell line does not express MT-3 and does not demonstrate vectorial active transport. Transfection of the MT-3 gene into the HK-2 cells restores vectorial active transport as evidenced by dome formation. This suggests that MT-3 is involved in mesenchymal to epithelial transition (MET), the reverse of EMT, and promotes and epithelial phenotype. The goals of the present study were to examine the role of growth media composition on classic EMT responses, quantitatively evaluate the expression levels of
E- and N-
cadherin, define the functional epitope of MT-3 that mediates MET in HK-2 cells, and identify proteins that interact with MT-3 to promote epithelial features in the proximal tubule. It was shown that both
E- and N-
cadherin mRNA and protein are expressed in the human renal proximal tubule. Based on the pattern of
cadherin expression, vectorial active transport, and transepithelial resistance, it seems that the HK-2 cell line has already undergone many of the early features associated with EMT. Our data indicates the unique, six amino acid C-terminal sequence of MT-3 is required to induce MET in HK-2 cells. A combination of co-immunoprecipitation and western blotting indicate that MT-3 interacts with myosin-IIa, β-actin, enolase-1, tropomyosin-3, and aldolase-a in vitro. Together, the data suggests the HK-2 cell line can be an effective model to study later stages in the conversion of the renal epithelial cell to a mesenchymal cell and when transfected with MT-3 it may be an effective model to study the process of MET. MT-3 protein-protein interactions provide insight into the potential mechanism by which MT-3 promotes cytoskeletal organization in non-diseased epithelial proximal tubule cells and offers the opportunity to investigate these interactions under pathological conditions.
Advisors/Committee Members: Scott H. Garrett.
Subjects/Keywords: Cadmium; E-cadherin; Kidney Disease; MT-3; N-cadherin; Proximal Tubule
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APA ·
Chicago ·
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Manager
APA (6th Edition):
Nore, A. M. (2015). Regulation Of Vectorial Active Transport In Human Proximal Tubule Cells By MT-3: The Role Of The C-Terminal Domain On E-And N-Cadherin Expression And The Confirmation Of Protein-Protein Interactions. (Doctoral Dissertation). University of North Dakota. Retrieved from https://commons.und.edu/theses/1938
Chicago Manual of Style (16th Edition):
Nore, Andrea Marie. “Regulation Of Vectorial Active Transport In Human Proximal Tubule Cells By MT-3: The Role Of The C-Terminal Domain On E-And N-Cadherin Expression And The Confirmation Of Protein-Protein Interactions.” 2015. Doctoral Dissertation, University of North Dakota. Accessed January 19, 2021.
https://commons.und.edu/theses/1938.
MLA Handbook (7th Edition):
Nore, Andrea Marie. “Regulation Of Vectorial Active Transport In Human Proximal Tubule Cells By MT-3: The Role Of The C-Terminal Domain On E-And N-Cadherin Expression And The Confirmation Of Protein-Protein Interactions.” 2015. Web. 19 Jan 2021.
Vancouver:
Nore AM. Regulation Of Vectorial Active Transport In Human Proximal Tubule Cells By MT-3: The Role Of The C-Terminal Domain On E-And N-Cadherin Expression And The Confirmation Of Protein-Protein Interactions. [Internet] [Doctoral dissertation]. University of North Dakota; 2015. [cited 2021 Jan 19].
Available from: https://commons.und.edu/theses/1938.
Council of Science Editors:
Nore AM. Regulation Of Vectorial Active Transport In Human Proximal Tubule Cells By MT-3: The Role Of The C-Terminal Domain On E-And N-Cadherin Expression And The Confirmation Of Protein-Protein Interactions. [Doctoral Dissertation]. University of North Dakota; 2015. Available from: https://commons.und.edu/theses/1938
Vanderbilt University
6.
Stoops, Sydney Lear.
Discovery, Optimization, and Understanding the Mechanism of Action of Small Molecules that Restore E-cadherin Expression.
Degree: PhD, Pharmacology, 2012, Vanderbilt University
URL: http://hdl.handle.net/1803/11403
► E-cadherin is a transmembrane protein that maintains intercellular contacts and cellular polarity in epithelial tissues. The down-regulation of E-cadherin is thought to aid in the…
(more)
▼ E-
cadherin is a transmembrane protein that maintains intercellular contacts and cellular polarity in epithelial tissues. The down-regulation of
E-
cadherin is thought to aid in the induction of an epithelial-to-mesenchymal (EMT) transition resulting in an increased potential for invasion into surrounding tissues and entry into the bloodstream. Loss of
E-
cadherin has been observed in a variety of human tumors resulting from somatic mutations, chromosomal deletions, proteolytic cleavage of
E-
cadherin, and most commonly silencing of the CDH1 gene promoter.
A novel High-throughput screen was developed to identify small molecules that restored
E-
cadherin expression in the SW620 cell line followed by medicinal chemistry employing iterative analog library synthesis to better identify the structure-activity relationship. Preliminary optimization of the screening hit has shown it is possible to synthesize small molecules that have an improved ability to restore
E-
cadherin expression compared to the initial screening hits.
Recent endeavors have been taken to elucidate the mechanism of action of these small molecules to restore
E-
cadherin expression. Quantitative PCR analysis has shown that
E-
cadherin mRNA expression occurs after 3 hours of treatment with active analogs, suggesting the small molecules are altering transcription of the CDH1 gene. This was supported by experiments conducted using various plasmid constructs containing truncated segments of the
E-
cadherin promoter region and luciferase reporter. It was shown that active analogs had a significant increase in luciferase activity as compared to DMSO or an inactive analog, which were used as controls. More specifically, we were able to narrow the site of action the active analogs to a 200 bp fragment of the
E-
cadherin promoter region.
Elucidation of the mechanism of action will aid in identifying the novel molecular target. Such information would allow for further development of more efficacious and potent small molecules as well as further research to understand the importance of this interaction in the role of EMT and as a therapeutic target.
Advisors/Committee Members: Professor Robert Coffey (committee member), Professor Stephen Fesik (committee member), Professor Lawrence Marnett (committee member), Professor Albert Reynolds (committee member), Professor Craig Lindsley (committee member), Professor Brian Wadzinski (Committee Chair).
Subjects/Keywords: EMT; E-Cadherin; Epithelial-Mesenchymal Transition
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APA ·
Chicago ·
MLA ·
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CSE |
Export
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Manager
APA (6th Edition):
Stoops, S. L. (2012). Discovery, Optimization, and Understanding the Mechanism of Action of Small Molecules that Restore E-cadherin Expression. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://hdl.handle.net/1803/11403
Chicago Manual of Style (16th Edition):
Stoops, Sydney Lear. “Discovery, Optimization, and Understanding the Mechanism of Action of Small Molecules that Restore E-cadherin Expression.” 2012. Doctoral Dissertation, Vanderbilt University. Accessed January 19, 2021.
http://hdl.handle.net/1803/11403.
MLA Handbook (7th Edition):
Stoops, Sydney Lear. “Discovery, Optimization, and Understanding the Mechanism of Action of Small Molecules that Restore E-cadherin Expression.” 2012. Web. 19 Jan 2021.
Vancouver:
Stoops SL. Discovery, Optimization, and Understanding the Mechanism of Action of Small Molecules that Restore E-cadherin Expression. [Internet] [Doctoral dissertation]. Vanderbilt University; 2012. [cited 2021 Jan 19].
Available from: http://hdl.handle.net/1803/11403.
Council of Science Editors:
Stoops SL. Discovery, Optimization, and Understanding the Mechanism of Action of Small Molecules that Restore E-cadherin Expression. [Doctoral Dissertation]. Vanderbilt University; 2012. Available from: http://hdl.handle.net/1803/11403
Universidade Nova
7.
Marques, Filipa Gil.
The involvement of CDH1 in cancer angiogenesis.
Degree: 2011, Universidade Nova
URL: http://www.rcaap.pt/detail.jsp?id=oai:run.unl.pt:10362/6645
► Dissertação para obtenção do Grau de Mestre em Biotecnologia
Cancer is one of the leading causes of death worldwide. Biological hallmarks such as induced and…
(more)
▼ Dissertação para obtenção do Grau de Mestre em
Biotecnologia
Cancer is one of the leading causes of death worldwide. Biological hallmarks such as induced and sustained angiogenesis are implicated in tumour progression, as well as invasion and metastasis which are the major causes of cancer-related mortality. E-Cadherin impairment on the cell membrane is intimately related with invasion and metastasis. Also, increased levels of vascular endothelial growth factor (VEGF), an angiogenic marker, and its receptor on the plasma membrane can be implicated in tumour progression.
This work was focused on how the inactivation of E-Cadherin, a molecule associated to an invasive phenotype can be related with angiogenesis, probably through VEGF-A expression.
Two different cell lines without expression of E-Cadherin and stably transduced to express wild-type (WT) E-Cadherin were used to carry out this study: AGS Par/WT (from stomach) and MDA-435 Mock/WT (from breast). Immunohistochemical staining was performed to determine the cellular localization and western blot analysis was performed to assess the expression levels of E-Cadherin. VEGFA mRNA levels were assessed by quantitative Real-time PCR. Additionally, we determined the levels phosphorylated (phospho) ERK1/2, as well as the expression levels of total ERK1/2. To study the angiogenic role of E-cadherin the chick embryo Chorioallantoic Membrane (CAM) assay was used. We characterise in vivo the different cell lines concerning both angiogenic and tumorigenic responses dependent on E-Cadherin.
Only cell lines stably expressing WT human E-Cadherin showed levels of expression of this protein at the cell membrane regardless of their tissue of origin. In vitro, AGS and MDA-435 cells expressing WT E-Cadherin revealed an increased expression of VEGFA in comparison to the control although not statically significant. In addition, both phospho-ERK1/2 and total ERK1/2 presented similar levels of expression regardless of the tissue of origin and E-Cadherin expression. Both angiogenic and tumorigenic responses in AGS WT was significantly increased in comparison to the control. The MDA-435 WT cells revealed increased tumorigenic response in comparison to the control. Overall, these results suggest that E-Cadherin expression is important for micro-tumour formation as well as for neovascularisation but this effect is dependent on the in vivo context.
Advisors/Committee Members: Seruca, Raquel.
Subjects/Keywords: Cancer; E-cadherin; (Tumour-) Angiogenesis; VEGF-A
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APA (6th Edition):
Marques, F. G. (2011). The involvement of CDH1 in cancer angiogenesis. (Thesis). Universidade Nova. Retrieved from http://www.rcaap.pt/detail.jsp?id=oai:run.unl.pt:10362/6645
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Marques, Filipa Gil. “The involvement of CDH1 in cancer angiogenesis.” 2011. Thesis, Universidade Nova. Accessed January 19, 2021.
http://www.rcaap.pt/detail.jsp?id=oai:run.unl.pt:10362/6645.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Marques, Filipa Gil. “The involvement of CDH1 in cancer angiogenesis.” 2011. Web. 19 Jan 2021.
Vancouver:
Marques FG. The involvement of CDH1 in cancer angiogenesis. [Internet] [Thesis]. Universidade Nova; 2011. [cited 2021 Jan 19].
Available from: http://www.rcaap.pt/detail.jsp?id=oai:run.unl.pt:10362/6645.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Marques FG. The involvement of CDH1 in cancer angiogenesis. [Thesis]. Universidade Nova; 2011. Available from: http://www.rcaap.pt/detail.jsp?id=oai:run.unl.pt:10362/6645
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
University of Toronto
8.
Fiorino, Cara Erica.
Examining Novel Factors that Influence Contact-dependent Osteoblast and Osteoclast Differentiation.
Degree: PhD, 2016, University of Toronto
URL: http://hdl.handle.net/1807/76405
► A dynamic equilibrium between bone destruction by osteoclasts and bone formation by osteoblasts is responsible for the maintenance of bone integrity, mineral homeostasis and protection…
(more)
▼ A dynamic equilibrium between bone destruction by osteoclasts and bone formation by osteoblasts is responsible for the maintenance of bone integrity, mineral homeostasis and protection from bone-related disease. As such, the focus of this work was to examine novel factors contributing to the contact-dependent differentiation of osteoblasts and osteoclasts. Osteoblast differentiation and maturation is stimulated by multiple external factors, two of which are ascorbic acid (AA) and bone morphogenetic protein-2 (BMP-2). Utilizing MC3T3-E1 cells and primary murine osteoblasts, we identified a novel role for EB1, a microtubule plus-end binding protein, during osteoblast differentiation. AA-stimulation strongly induced EB1 expression and EB1 knockdown significantly impaired the osteoblast differentiation program in both AA- and BMP-2-induced osteoblasts. Furthermore, we identified that EB1 function was important for the global stability of -catenin, a major signaling molecule in osteoblasts. Lastly, the influence of
E-
cadherin, a cell-cell adhesion and recognition molecule, was investigated in AA-stimulated osteoblasts. Up-regulation of Cdh1 (
E-
cadherin) paralleled that of Catnb (beta-catenin), and
E-
cadherin blocking antibody treatment dampened osteoblast-specific gene expression.
E-
cadherin is also expressed in monocyte/macrophage cells, which are precursors to osteoclasts. Receptor activator of nuclear factor-ÎşB ligand (RANKL)-stimulated osteoclast differentiation involves a period of precursor expansion followed by multiple fusion events to generate a multinucleated osteoclast. Interestingly, our results indicated that
E-
cadherin participated in early precursor interaction/recognition rather than during periods of osteoclast fusion. In both RAW 264.7 cells and primary murine macrophages,
E-
cadherin expression and surface localization was highest during early osteoclast differentiation. Utilizing
E-
cadherin blocking antibodies prior to the onset of fusion delayed osteoclast-specific gene expression and significantly impaired multinucleated osteoclast formation. Long-term imaging revealed that blocking
E-
cadherin function prolonged the proliferative phase of the precursor population while concomitantly decreasing the proportion of migrating precursors; the lamellipodium and polarized membrane extensions were identified as principal sites of fusion, establishing migration as a requirement for osteoclast differentiation.
This work characterizes EB1 and
E-
cadherin function during osteoblast differentiation and the
E-
cadherin-mediated transition from proliferative to migratory activities during osteoclast differentiation. Taken together, both studies highlight the value of exploring the early intra- and intercellular events that direct osteoblast and osteoclast differentiation.
Advisors/Committee Members: Harrison, Rene E., Cell and Systems Biology.
Subjects/Keywords: differentiation; EB1; E-cadherin; osteoblast; osteoclast; 0379
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APA (6th Edition):
Fiorino, C. E. (2016). Examining Novel Factors that Influence Contact-dependent Osteoblast and Osteoclast Differentiation. (Doctoral Dissertation). University of Toronto. Retrieved from http://hdl.handle.net/1807/76405
Chicago Manual of Style (16th Edition):
Fiorino, Cara Erica. “Examining Novel Factors that Influence Contact-dependent Osteoblast and Osteoclast Differentiation.” 2016. Doctoral Dissertation, University of Toronto. Accessed January 19, 2021.
http://hdl.handle.net/1807/76405.
MLA Handbook (7th Edition):
Fiorino, Cara Erica. “Examining Novel Factors that Influence Contact-dependent Osteoblast and Osteoclast Differentiation.” 2016. Web. 19 Jan 2021.
Vancouver:
Fiorino CE. Examining Novel Factors that Influence Contact-dependent Osteoblast and Osteoclast Differentiation. [Internet] [Doctoral dissertation]. University of Toronto; 2016. [cited 2021 Jan 19].
Available from: http://hdl.handle.net/1807/76405.
Council of Science Editors:
Fiorino CE. Examining Novel Factors that Influence Contact-dependent Osteoblast and Osteoclast Differentiation. [Doctoral Dissertation]. University of Toronto; 2016. Available from: http://hdl.handle.net/1807/76405
University of Edinburgh
9.
Teo, Katy Ann.
Elucidating biological mechanisms associated with invasive lobular carcinoma of the breast.
Degree: PhD, 2017, University of Edinburgh
URL: http://hdl.handle.net/1842/23628
► Breast cancer is a heterogeneous disease, and can be classified according to histological subtypes based on cellular morphology. Invasive ductal carcinoma (IDC) and invasive lobular…
(more)
▼ Breast cancer is a heterogeneous disease, and can be classified according to histological subtypes based on cellular morphology. Invasive ductal carcinoma (IDC) and invasive lobular carcinoma (ILC) are the most common histological subtypes, accounting for approximately 80% and 12% of cases respectively. ILC exhibits a number of distinct clinico-pathological features in comparison with IDC, and is understudied as a breast cancer subtype. ILC tumours are typically oestrogen receptor positive, HER2 negative, and frequently demonstrate early loss of Ecadherin expression, which is a hallmark of the lobular phenotype. ILC is presently treated in a similar manner to IDC, with treatment generally directed against hormone receptors. Upon acquisition of hormone resistance, limited secondary options are available; patients are rarely candidates for agents targeting HER2, and are recognised to be poorly responsive to chemotherapeutics. We therefore need to advance our understanding of lobular tumour biology, in order to identify suitable biomarkers that will guide the development of targeted therapies for ILC patients. As protein expression levels determine cellular phenotype, a protein-based approach has the potential to provide biologically relevant insight into the mechanisms driving ILC. A range of protein analysis platforms, including reverse phase protein array, label-free mass spectrometry and immunohistochemistry, were therefore used to elucidate biological mechanisms active in the ILC subtype. Such experiments led to the identification of activated PI3K-Akt signalling in mouse and human ILC, suggesting that inhibition of this pathway may be an effective treatment strategy in lobular breast cancer. Preliminary evidence of differences in cytoskeletal and extracellular matrix (ECM) proteins was also acquired, providing an interesting basis for future research. A further major strand of this project was the development of in vitro and in vivo tools, to facilitate further interrogation of lobular biology. This included determination of a representative mouse model of ILC, and generation of primary cancer cells and cancer-associated fibroblasts (CAFs) from patient-derived material. Analysis of CAFS showed differential expression of ECM-associated genes, consistent with proteomic analyses. In addition, a tissue micro-array (TMA) comprising primary ILC and IDC tumours, with associated clinical data, was developed. Immunohistochemical staining of the TMA identified a potential role for IGF-1 pathway signalling in ILC, with increased expression of IGF-1 ligand associating with increased tumour size and metastasis in ILC patients. Taken together, the generation and validation of a range of useful tools in the course of this work has provided useful insight into the unique biology of ILC.
Subjects/Keywords: 616.99; breast cancer; lobular; E-cadherin
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APA (6th Edition):
Teo, K. A. (2017). Elucidating biological mechanisms associated with invasive lobular carcinoma of the breast. (Doctoral Dissertation). University of Edinburgh. Retrieved from http://hdl.handle.net/1842/23628
Chicago Manual of Style (16th Edition):
Teo, Katy Ann. “Elucidating biological mechanisms associated with invasive lobular carcinoma of the breast.” 2017. Doctoral Dissertation, University of Edinburgh. Accessed January 19, 2021.
http://hdl.handle.net/1842/23628.
MLA Handbook (7th Edition):
Teo, Katy Ann. “Elucidating biological mechanisms associated with invasive lobular carcinoma of the breast.” 2017. Web. 19 Jan 2021.
Vancouver:
Teo KA. Elucidating biological mechanisms associated with invasive lobular carcinoma of the breast. [Internet] [Doctoral dissertation]. University of Edinburgh; 2017. [cited 2021 Jan 19].
Available from: http://hdl.handle.net/1842/23628.
Council of Science Editors:
Teo KA. Elucidating biological mechanisms associated with invasive lobular carcinoma of the breast. [Doctoral Dissertation]. University of Edinburgh; 2017. Available from: http://hdl.handle.net/1842/23628
Queens University
10.
Vanderlee, Amanda.
Reciprocal Regulation of E-Cadherin and SHP2 by the Extracellular CA2+-Sensing Receptor in Colonic Epithelial Adenocarcinoma Cells
.
Degree: Physiology, 2009, Queens University
URL: http://hdl.handle.net/1974/1943
► Colon cancer is characterized by the progressive loss of E-cadherin, a Ca2+-dependent adherens junction component and epithelial marker. Furthermore, inhibition of the phosphatase SHP2, essential…
(more)
▼ Colon cancer is characterized by the progressive loss of E-cadherin, a Ca2+-dependent adherens junction component and epithelial marker. Furthermore, inhibition of the phosphatase SHP2, essential in the cell survival signaling via the epidermal growth factor receptor pathway, has been shown to upregulate E-cadherin in breast cancer cell lines. This suggests that unregulated increases in SHP2 may promote a cancer cell phenotype. The aim of this study was to define molecular mechanisms by which dietary Ca2+ is chemoprotective against colon cancer. The extracellular Ca2+-sensing receptor (CaSR) has been implicated in this process and we speculated that there was a relationship between CaSR activation and E-cadherin and SHP2 expression levels on colonic epithelia. A colonic adenocarcinoma cell line which lacks endogenous E-cadherin expression, SW480, was used as a model cell. CaSR levels were manipulated by transient transfection and E-cadherin and SHP2 expression levels were determined by Western blotting. The E-cadherin expression pattern was also assessed with RT-PCR and immunocytochemistry. We found that after CaSR activation via Ca2+ or other known CaSR agonists (neomycin sulphate, spermine), E-cadherin expression was increased and SHP2 expression was decreased. However, the E-cadherin expression pattern was altered in the presence of a dominant-negative CaSR (R185Q). Furthermore, pharmacological inhibition of p38 MAPK inhibited CaSR-mediated increases of E-cadherin protein in SW480 cells. Inhibition of p38 MAPK had no effect on CaSR-stimulation of E-cadherin transcript or promoter activity. SHP2 decreases usually seen after Ca2+-treatment were reduced after pharmacological inhibition of JNK in the presence of high Ca2+. CaSR activation also increased cell-cell adherence as assessed by electronic cell sizing and this adherence was lost when both CaSR-mediated changes in E-cadherin and SHP2 expression were inhibited. We conclude that CaSR activation in colonic epithelial cancer cells stimulated E-cadherin increases, through a mechanism involving p38 MAPK, as well as inhibited SHP2 expression, through a JNK-mediated mechanism. Further, these protein changes post-CaSR activation cause an increase in cell-cell adherence. Our results suggest that the chemoprotective nature of dietary Ca2+ supplements may involve reciprocal regulation of E-cadherin and SHP2 via the CaSR.
Subjects/Keywords: E-Cadherin
;
CaSR
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APA (6th Edition):
Vanderlee, A. (2009). Reciprocal Regulation of E-Cadherin and SHP2 by the Extracellular CA2+-Sensing Receptor in Colonic Epithelial Adenocarcinoma Cells
. (Thesis). Queens University. Retrieved from http://hdl.handle.net/1974/1943
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Vanderlee, Amanda. “Reciprocal Regulation of E-Cadherin and SHP2 by the Extracellular CA2+-Sensing Receptor in Colonic Epithelial Adenocarcinoma Cells
.” 2009. Thesis, Queens University. Accessed January 19, 2021.
http://hdl.handle.net/1974/1943.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Vanderlee, Amanda. “Reciprocal Regulation of E-Cadherin and SHP2 by the Extracellular CA2+-Sensing Receptor in Colonic Epithelial Adenocarcinoma Cells
.” 2009. Web. 19 Jan 2021.
Vancouver:
Vanderlee A. Reciprocal Regulation of E-Cadherin and SHP2 by the Extracellular CA2+-Sensing Receptor in Colonic Epithelial Adenocarcinoma Cells
. [Internet] [Thesis]. Queens University; 2009. [cited 2021 Jan 19].
Available from: http://hdl.handle.net/1974/1943.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Vanderlee A. Reciprocal Regulation of E-Cadherin and SHP2 by the Extracellular CA2+-Sensing Receptor in Colonic Epithelial Adenocarcinoma Cells
. [Thesis]. Queens University; 2009. Available from: http://hdl.handle.net/1974/1943
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
University of British Columbia
11.
Park, Se Hyung.
Estrogen in ovarian cancer cell metastasis.
Degree: PhD, Reproductive and Developmental Sciences, 2008, University of British Columbia
URL: http://hdl.handle.net/2429/1287
► Benign ovarian tumors and majority of epithelial ovarian cancers possess steroid receptors including estrogen receptors (ERs). However, the estrogen-ER signaling in ovarian carcinomas is not…
(more)
▼ Benign ovarian tumors and majority of epithelial ovarian cancers possess steroid receptors including estrogen receptors (ERs). However, the estrogen-ER signaling in ovarian carcinomas is not completely understood. Tumorigenesis is a multiple-step process involving dysregulated cell growth and metastasis. Tumor cells acquire the capacity of migration and invasion by temporal phenotypical and genotypical changes termed epithelial-mesenchymal transition (EMT). Considerable evidence implicates a mitogenic action of estrogen in early ovarian carcinogenesis. In contrast, its influence in the metastatic cascade of ovarian tumor cells remains obscure. In this study, I have focused on the role of 17β-estradiol (E2) in ovarian tumorigenesis. EMT related genes including E-cadherin, Snail, Slug, and Twist were examined. E2 treatment led to clear morphological changes and an enhanced cell migratory propensity. These morphologic and functional alterations were associated with changes in the abundance of EMT-related genes. Upon E2 stimulation, expression and promoter activity of the epithelial marker E-cadherin was strikingly suppressed, whereas EMT-associated transcription factors Snail and Slug were significantly up-regulated. This up-regulation was attributed to the increase in gene transcription activated by E2. Depletion of the endogenous Snail or Slug using small interfering RNA (siRNA) attenuated E2-mediated control in E-cadherin. In addition, the E2-induced cell migration was neutralized by Snail and Slug siRNAs, implying that both transcription factors are indispensable for the pro-metastatic actions of E2. Importantly, by using selective ER agonists as well as over-expression and siRNA approaches, it was identified that E2 triggered the metastatic behaviors exclusively through an ER⍺-dependent pathway. In contrast, overexpression of ERβ opposed the phenotypic changes and down-regulation of E-cadherin induced by ER⍺. In addition, microarray analysis was performed to characterize more putative downstream mediators of E2. Expression levels of 486 genes were found to be altered by at least 50% upon E2 treatment, and included several genes involved in oncogenesis, cell cycle control, apoptosis, signal transduction and the gene expression machinery. These candidate genes may be valuable for better delineating the ER pathways and functions. In summary, this study provides compelling arguments that estrogen can potentiate tumor progression by EMT induction, and highlight the crucial role of ER⍺ in ovarian tumorigenesis.
Subjects/Keywords: Estrogen; E-cadherin
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APA (6th Edition):
Park, S. H. (2008). Estrogen in ovarian cancer cell metastasis. (Doctoral Dissertation). University of British Columbia. Retrieved from http://hdl.handle.net/2429/1287
Chicago Manual of Style (16th Edition):
Park, Se Hyung. “Estrogen in ovarian cancer cell metastasis.” 2008. Doctoral Dissertation, University of British Columbia. Accessed January 19, 2021.
http://hdl.handle.net/2429/1287.
MLA Handbook (7th Edition):
Park, Se Hyung. “Estrogen in ovarian cancer cell metastasis.” 2008. Web. 19 Jan 2021.
Vancouver:
Park SH. Estrogen in ovarian cancer cell metastasis. [Internet] [Doctoral dissertation]. University of British Columbia; 2008. [cited 2021 Jan 19].
Available from: http://hdl.handle.net/2429/1287.
Council of Science Editors:
Park SH. Estrogen in ovarian cancer cell metastasis. [Doctoral Dissertation]. University of British Columbia; 2008. Available from: http://hdl.handle.net/2429/1287
12.
Vlug, E.J.
Loss of cadherin-based cell adhesion and the progression of Invasive Lobular Breast Cancer.
Degree: 2015, Universiteit Utrecht
URL: http://dspace.library.uu.nl:8080/handle/1874/310469
► Lobular breast cancer is a type of breast cancer that is histologically characterized by a noncohesive growth pattern of small regular cells, where single cells…
(more)
▼ Lobular breast cancer is a type of breast cancer that is histologically characterized by a noncohesive growth pattern of small regular cells, where single cells infiltrate as one-layered strands of cells. This noncohesive growth pattern is due to inactivation of the
E-
cadherin complex and a subsequent lack of cell-cell adhesion. Currently there is no specific treatment for lobular breast cancer, and metastatic disease cannot be cured.
By aiming to gain knowledge about the key signaling pathways to enable future development of targeted new therapies that can successfully treat lobular breast cancer, we have learned about the role of the
E-
cadherin complex member α-catenin and the yes-associated protein (YAP) in breast cancer progression. Overall this thesis describes different aspects of lobular breast cancer, like pathology, etiology, subtypes, markers and signaling pathways involved in tumor progression.
Advisors/Committee Members: Diest, P.J. van, Derksen, P.W.B..
Subjects/Keywords: lobular breast cancer; invasive lobular carcinoma; E-cadherin; α-catenin; E-cadherin; adherens junction
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APA ·
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APA (6th Edition):
Vlug, E. J. (2015). Loss of cadherin-based cell adhesion and the progression of Invasive Lobular Breast Cancer. (Doctoral Dissertation). Universiteit Utrecht. Retrieved from http://dspace.library.uu.nl:8080/handle/1874/310469
Chicago Manual of Style (16th Edition):
Vlug, E J. “Loss of cadherin-based cell adhesion and the progression of Invasive Lobular Breast Cancer.” 2015. Doctoral Dissertation, Universiteit Utrecht. Accessed January 19, 2021.
http://dspace.library.uu.nl:8080/handle/1874/310469.
MLA Handbook (7th Edition):
Vlug, E J. “Loss of cadherin-based cell adhesion and the progression of Invasive Lobular Breast Cancer.” 2015. Web. 19 Jan 2021.
Vancouver:
Vlug EJ. Loss of cadherin-based cell adhesion and the progression of Invasive Lobular Breast Cancer. [Internet] [Doctoral dissertation]. Universiteit Utrecht; 2015. [cited 2021 Jan 19].
Available from: http://dspace.library.uu.nl:8080/handle/1874/310469.
Council of Science Editors:
Vlug EJ. Loss of cadherin-based cell adhesion and the progression of Invasive Lobular Breast Cancer. [Doctoral Dissertation]. Universiteit Utrecht; 2015. Available from: http://dspace.library.uu.nl:8080/handle/1874/310469
13.
Kale, Girish.
Etude de l'effet de l'orientation des forces sur la dynamique de l'adhésion au cours de la morphogenèse tissulaire : Studying the effect of oriented forces on adhesion dynamics during tissue morphogenesis.
Degree: Docteur es, Biologie du développement, 2017, Aix Marseille Université
URL: http://www.theses.fr/2017AIXM0072
► Les organismes multicellulaires, tels les mammifères, possèdent plusieurs organes constitués de couches de cellules, par exemple la peau ou l’intestin. Ces couches, appelées épithelia, fonctionnent…
(more)
▼ Les organismes multicellulaires, tels les mammifères, possèdent plusieurs organes constitués de couches de cellules, par exemple la peau ou l’intestin. Ces couches, appelées épithelia, fonctionnent comme des barrières. Une protéine nommée E-Cadhérine agit comme une colle moléculaire et procure l’adhésion cellule-cellule qui est nécessaire à la fonction de barrière. Les épithelia changent aussi leur structure pendant le développement de l’organisme ou pendant les maladies. Nous étudions un exemple d’un tel changement structurel. Pendant le développement de la mouche du vinaigre, à un stade précis, le tissu épithélial change de forme au travers d’un réarrangement des cellules. C’est un procédé complexe, car les cellules doivent maintenir l’adhésion tout en échangeant de voisin. Les forces requises pour ce procédé sont générées par une activité et une distribution spécifiques des moteurs moléculaires nommés Myosine. Nous voulons comprendre comment la distribution de la Myosine change l’adhésion entre les cellules pour permettre cet échange de voisins. Nous répondons à cette question en changeant la distribution de la Myosine et en regardant l’effet sur la E-Cadhérine. Sur la base de nos expériences nous sommes à même de conclure que l’orientation des forces est un facteur important (et précédemment négligé) de leur effet sur l’adhésion.
Multicellular organisms, such as mammals, have several organs that are made of sheets of cells e.g. skin or intestine. These sheets, called epithelia, function as barriers. A protein called E-Cadherin acts as molecular glue and mediates cell-cell adhesion that is essential for barrier function. Epithelia also change their structure during organismal development or during diseases. We are looking at one such example of structural change. During embryonic development of fruit fly, at specific stage, epithelial tissue changes shape due to cell mixing. It is a complex process, as cells have to maintain adhesion all around while they exchange neighbors. The forces required for this process are generated by specific activity and distribution of molecular motors, called Myosin. We want to understand how Myosin distribution changes adhesion between cells to allow neighbor exchange. We answer this question by changing the distribution of Myosin and seeing its effects on E-Cadherin. Based on our experiments we could conclude that orientation of forces is an important (and previously neglected) factor to predict their effects on adhesion.
Advisors/Committee Members: Lecuit, Thomas (thesis director), Lenne, Pierre-François (thesis director).
Subjects/Keywords: E-Cadhérine; Vinculine; Mechanosensor; E-Cadherin; Vinculin; Mechanosenor; 570
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APA ·
Chicago ·
MLA ·
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CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Kale, G. (2017). Etude de l'effet de l'orientation des forces sur la dynamique de l'adhésion au cours de la morphogenèse tissulaire : Studying the effect of oriented forces on adhesion dynamics during tissue morphogenesis. (Doctoral Dissertation). Aix Marseille Université. Retrieved from http://www.theses.fr/2017AIXM0072
Chicago Manual of Style (16th Edition):
Kale, Girish. “Etude de l'effet de l'orientation des forces sur la dynamique de l'adhésion au cours de la morphogenèse tissulaire : Studying the effect of oriented forces on adhesion dynamics during tissue morphogenesis.” 2017. Doctoral Dissertation, Aix Marseille Université. Accessed January 19, 2021.
http://www.theses.fr/2017AIXM0072.
MLA Handbook (7th Edition):
Kale, Girish. “Etude de l'effet de l'orientation des forces sur la dynamique de l'adhésion au cours de la morphogenèse tissulaire : Studying the effect of oriented forces on adhesion dynamics during tissue morphogenesis.” 2017. Web. 19 Jan 2021.
Vancouver:
Kale G. Etude de l'effet de l'orientation des forces sur la dynamique de l'adhésion au cours de la morphogenèse tissulaire : Studying the effect of oriented forces on adhesion dynamics during tissue morphogenesis. [Internet] [Doctoral dissertation]. Aix Marseille Université 2017. [cited 2021 Jan 19].
Available from: http://www.theses.fr/2017AIXM0072.
Council of Science Editors:
Kale G. Etude de l'effet de l'orientation des forces sur la dynamique de l'adhésion au cours de la morphogenèse tissulaire : Studying the effect of oriented forces on adhesion dynamics during tissue morphogenesis. [Doctoral Dissertation]. Aix Marseille Université 2017. Available from: http://www.theses.fr/2017AIXM0072
14.
Levayer, Romain.
Modulation of intercellular adhesion during epithelial morphogenesis : Experimental study of the behaviour and the evaporation of a liquid fuel film in the presence of a flame.
Degree: Docteur es, Biologie, Spécialité biologie du développement, 2011, Aix-Marseille 2
URL: http://www.theses.fr/2011AIX22076
► Les épithéliums jouent le rôle fondamental de barrière physique et chimique chez les Métazoaires. Les jonctions adhérentes, par le biais de la protéine transmembranaire E-cadhérine…
(more)
▼ Les épithéliums jouent le rôle fondamental de barrière physique et chimique chez les Métazoaires. Les jonctions adhérentes, par le biais de la protéine transmembranaire E-cadhérine (E-cad), assurent une grande partie de l’adhésion intercellulaire. Malgré cette robustesse, les épithéliums peuvent subir des remodelages considérables pendant l’embryogenèse ou la cicatrisation. Lors de la gastrulation de l’embryon de Drosophile, l’épithélium ventro-latéral (la bandelette germinale) subit une élongation le long de l’axe antéropostérieur induite par l’intercalation cellulaire. Le remodelage polarisé des jonctions cellulaires est à la base de ce phénomène: les jonctions parallèles à l’axe dorsoventral (DV) rétrécissent et forment de manière irréversible de nouvelles jonctions parallèles à l’axe antéropostérieur (AP). Ce remodelage dépend de l’enrichissement du moteur moléculaire Myosine II (MyoII) dans les jonctions DV, qui induit une anisotropie de tension. Les protéines des jonctions adhérentes (E-cad, β-catenin) sont, elles aussi, polarisées : elles sont enrichies dans les jonctions AP. Néanmoins, nous ne savions pas si cette polarité de l’adhésion avait un rôle dans le remodelage des jonctions, et nous ne connaissions pas les mécanismes contrôlant cette localisation asymétrique. L’un des mécanismes les mieux connus de la modulation de l’adhésion cellulaire est l’endocytose des protéines d’adhésion. A ce titre, je me suis intéressé au rôle de l’endocytose Clathrine dépendante (ECD) pendant l’intercalation cellulaire. J’ai ainsi pu montrer que l’ECD de E-cad est régulée à la hausse dans la bandelette germinale au niveau jonctionnelle, plus particulièrement au niveau des jonctions DV (qui rétrécissent). L’ECD d’E-cad est nécessaire à l’intercalation et à la distribution polarisée d’E-cad. Elle est régulée par l’organisation de l’actine: la formine Diaphanous ainsi que le moteur moléculaire Myosine II accélèrent le recrutement de la machinerie d’endocytose (AP2 et Clathrine) et régulent la polarité de l’ECD dans l’embryon. Elles sont contrôlées par RhoGEF2, qui est enrichie dans les jonctions DV, et induisent l’endocytose par un mécanisme de clustering latéral d’E-cad. Dans la seconde partie de ma thèse, je me suis intéressé au couplage entre E-cad et la dynamique de MyoII. En effet, l’intercalation dépend aussi de flux contractiles de MyoII qui ont lieu préférentiellement en direction des jonctions DV. J’ai ainsi pu montrer que la direction des flux est induite par les anisotropies de forces d’ancrage de MyoII. Les faibles niveaux d’E-cad et le fort taux d’endocytose dans les jonctions DV augmentent la probabilité de générer une anisotropie d’ancrage et induisent davantage de flux de MyoII vers les jonctions DV. Ce projet met en lumière le rôle fondamental du couplage entre E-cad et MyoII dans la régulation de la morphogenèse.
Epithelia build up strong mechanical and chemichal barriers in Metazoans. Adherens junctions, through the adhesion provided by the transmembrane protein E-cadherin (E-cad), are essential for…
Advisors/Committee Members: Lecuit, Thomas (thesis director).
Subjects/Keywords: Morphogenèse; Épithélium; E-cadherin; Actine; Myosine II; Endocytose; Clathrin; Flux; Morphogenesis; Epithelium; E-cadherin; Actin; Myosin II; Endocytosis; Clathrin; Flow
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APA (6th Edition):
Levayer, R. (2011). Modulation of intercellular adhesion during epithelial morphogenesis : Experimental study of the behaviour and the evaporation of a liquid fuel film in the presence of a flame. (Doctoral Dissertation). Aix-Marseille 2. Retrieved from http://www.theses.fr/2011AIX22076
Chicago Manual of Style (16th Edition):
Levayer, Romain. “Modulation of intercellular adhesion during epithelial morphogenesis : Experimental study of the behaviour and the evaporation of a liquid fuel film in the presence of a flame.” 2011. Doctoral Dissertation, Aix-Marseille 2. Accessed January 19, 2021.
http://www.theses.fr/2011AIX22076.
MLA Handbook (7th Edition):
Levayer, Romain. “Modulation of intercellular adhesion during epithelial morphogenesis : Experimental study of the behaviour and the evaporation of a liquid fuel film in the presence of a flame.” 2011. Web. 19 Jan 2021.
Vancouver:
Levayer R. Modulation of intercellular adhesion during epithelial morphogenesis : Experimental study of the behaviour and the evaporation of a liquid fuel film in the presence of a flame. [Internet] [Doctoral dissertation]. Aix-Marseille 2; 2011. [cited 2021 Jan 19].
Available from: http://www.theses.fr/2011AIX22076.
Council of Science Editors:
Levayer R. Modulation of intercellular adhesion during epithelial morphogenesis : Experimental study of the behaviour and the evaporation of a liquid fuel film in the presence of a flame. [Doctoral Dissertation]. Aix-Marseille 2; 2011. Available from: http://www.theses.fr/2011AIX22076
15.
Shafraz, Omer.
Biophysics of cadherin interactions and junction assembly.
Degree: 2018, Iowa State University
URL: https://lib.dr.iastate.edu/etd/17312
► Desmosomes are robust cell adhesion junctions that are composed of two transmembrane desmosomal cadherin proteins: desmoglein (Dsg) and desmocollin (Dsc). The extracellular regions of Dsc…
(more)
▼ Desmosomes are robust cell adhesion junctions that are composed of two transmembrane desmosomal cadherin proteins: desmoglein (Dsg) and desmocollin (Dsc). The extracellular regions of Dsc and Dsg form an adhesive interface between cells while their cytoplasmic tails links to the intracellular keratin filament network. This dissertation investigates how Dsc and Dsg assemble into desmosomes using single molecule force measurements with an Atomic Force Microscope (AFM) and cell-based fluorescence assays. In Chapter 1, I give a brief over view of the content of this dissertation and the principles of AFM force measurements. In Chapter 2, I characterize the binding of isoform 2 of desmosomal cadherins. I show that Dsc2 dimerizes homophilically in a Ca2+ and tryptophan-2 (W2) dependent fashion; this binding mechanism, called ‘strand-swap dimerization’ has previously been found with other cadherins. In contrast, Dsg2 forms Ca2+ and W2 independent heterophilic binding with Dsc2. In Chapter 3 of the thesis, I describe how Dsg2 is recruited to desmosome. I show that E-cadherin (Ecad), a classical cadherin, interacts with Dsg2 in a Ca2+ independent manner, via a conserved Leu 175 on the Ecad cis binding interface. Furthermore, we demonstrate that desmosome assembly is initiated at sites of Ecad trans homodimerization and that Ecad-L175 is required for efficient Dsg2 and desmoplakin (DP) recruitment. Our data suggest that Ecad trans interactions at nascent cell-cell contacts initiate the recruitment of Dsg2 through direct cis interactions with Ecad; consequently, Dsg2 binds to Dsc2 and mediate robust desmosome assembly. In the fourth Chapter of this thesis, I develop and use a fast fluorescence recovery after photobleaching (FRAP) method to identify the dynamics of the Ecads trafficking at cell-cell junctions. Our preliminary data suggests that Ecads are recycled in and out of the junction by vesicle fusion. The final Chapter summarizes the conclusions and I propose future directions for these projects.
Subjects/Keywords: AFM; Cadherin; Desmosome; E-cadherin; Biophysics; Physics
…show that E-cadherin (Ecad), a classical cadherin, interacts with Dsg2 in a Ca2… …include epithelial (E) and neuronal (N)
cadherin, have a conserved HAV… …HAV
motif 47,48 . Several studies have shown that the classical cadherin E-cadherin (… …x28;2017).
10. Kan, N. G. et al. Gene replacement reveals a specific role for E-cadherin in… …Larue, L., Ohsugi, M., Hirchenhain, J. & Kemler, R. E-cadherin null mutant embryos fail
to…
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APA (6th Edition):
Shafraz, O. (2018). Biophysics of cadherin interactions and junction assembly. (Thesis). Iowa State University. Retrieved from https://lib.dr.iastate.edu/etd/17312
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Shafraz, Omer. “Biophysics of cadherin interactions and junction assembly.” 2018. Thesis, Iowa State University. Accessed January 19, 2021.
https://lib.dr.iastate.edu/etd/17312.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Shafraz, Omer. “Biophysics of cadherin interactions and junction assembly.” 2018. Web. 19 Jan 2021.
Vancouver:
Shafraz O. Biophysics of cadherin interactions and junction assembly. [Internet] [Thesis]. Iowa State University; 2018. [cited 2021 Jan 19].
Available from: https://lib.dr.iastate.edu/etd/17312.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Shafraz O. Biophysics of cadherin interactions and junction assembly. [Thesis]. Iowa State University; 2018. Available from: https://lib.dr.iastate.edu/etd/17312
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
NSYSU
16.
Li, Wen-yuan.
Immunohistochemical study for DLK-1 expression in ovarian cancers.
Degree: Master, Biological Sciences, 2016, NSYSU
URL: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0806116-110828
► Ovarian carcinoma has poor prognosis with a high mortality rate in gynecologic malignancy. The epithelial ovarian cancers account for 90% of ovarian malignancy. They have…
(more)
▼ Ovarian carcinoma has poor prognosis with a high mortality rate in gynecologic malignancy. The epithelial ovarian cancers account for 90% of ovarian malignancy. They have been considered arising from the surface epithelium covering the ovary. The major types of epithelial ovarian cancers include serous, endometrioid, mucinous and clear cell carcinomas.
DLK-1(Delta-Like 1 Homolog) is a transmembranous and secreted protein belonging to the epidermal growth factor-like homeotic family. Although expressed widely during embryonic development, only few types of tissue retain DLK-1 expression in adults. DLK-1 plays important roles in regulating cell differentiation, such as adipogenesis and osteogenesis. Aberrant expression of DLK1 has been found in various types of human cancers, including neuroblastoma, hepatocellular carcinoma, glioma and prostate cancer, but its expression in ovarian cancer has not yet been studied.CD44 is known as a stem cell marker. Previous studies showed that CD44 expressed higher level in ovarian cancer tissues and has been identified as a biomarker of ovarian carcinoma. Vimentin is a type III intermediate filament protein that is widely expressed in mesenchymal tissue, and is considered an important marker for epithelial-mesenchymal transition (EMT).
E-
cadherin is widely expressed in epithelial cells and acts as a pivotal tumor suppressor. Loss of
E-
cadherin expression has been known to be involved in epithelial-mesenchymal transition.
This study was aimed to discover the significance of DLK-1 expression and its correlation with tumor stemness and EMT in various types of epithelial ovarian cancer. The expression of DLK-1, CD44, vimentin and
E-
cadherin were analyzed in 283 ovarian carcinomas by immunohistochemistry on tissue microarray. The result showed positive correlation among DLK-1, CD44 and Vimentin expressions (P ï¼ 0.01). Although there was no statistical significance (P ï¼ 0.237), a reversed correlation was noted between the expressions of DLK-1 and
E-
cadherin in ovarian carcinomas. Our study revealed that DLK-1 is overexpressed in epithelial ovarian cancers, especially in endometrioid carcinoma.
In summary, DLK-1 may correlate with EMT and tumor stemness of ovarian carcinoma. Further study is needed to assess the potential use of DLK-1 for therapeutic strategy and prognosis evaluation.
Advisors/Committee Members: Ming-Hong Tai (chair), Chen-Hsuan Wu (chair), Chao-Cheng Huang (committee member), Jiin-Tsuey Cheng (committee member).
Subjects/Keywords: E-cadherin; Vimentin; CD44; DLK-1; Ovarian carcinoma
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APA ·
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CSE |
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APA (6th Edition):
Li, W. (2016). Immunohistochemical study for DLK-1 expression in ovarian cancers. (Thesis). NSYSU. Retrieved from http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0806116-110828
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Li, Wen-yuan. “Immunohistochemical study for DLK-1 expression in ovarian cancers.” 2016. Thesis, NSYSU. Accessed January 19, 2021.
http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0806116-110828.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Li, Wen-yuan. “Immunohistochemical study for DLK-1 expression in ovarian cancers.” 2016. Web. 19 Jan 2021.
Vancouver:
Li W. Immunohistochemical study for DLK-1 expression in ovarian cancers. [Internet] [Thesis]. NSYSU; 2016. [cited 2021 Jan 19].
Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0806116-110828.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Li W. Immunohistochemical study for DLK-1 expression in ovarian cancers. [Thesis]. NSYSU; 2016. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0806116-110828
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
University of Otago
17.
Yajid, Aidy Irman.
Human Papillomavirus Type 16 E6 Regulation Of Human Adhesion Protein, E-cadherin
.
Degree: University of Otago
URL: http://hdl.handle.net/10523/5853
► HPV is a non-lytic virus that infects and replicates within keratinocytes in the skin. Persistent infection with high risk human papillomavirus (HPV) such as HPV…
(more)
▼ HPV is a non-lytic virus that infects and replicates within keratinocytes in the skin. Persistent infection with high risk human papillomavirus (HPV) such as HPV type 16 and 18 is associated with cervical cancer. Despite the expression of viral antigens during replication, the immune system is unable to efficiently clear HPV infection due to the presence of multiple evasion techniques deployed by this virus.
E-
cadherin loss is a common feature in high-risk HPV infected cells and is associated with a reduction in the number of Langerhans cells at the infection site. The ability of HVP16 to reduce
E-
cadherin expression is directly linked to the expression of E6 and E7.
We utilised HCT116 with stable HPV16 E6 expression to study mechanisms involved in E6 regulation of surface
E-
cadherin. We examined regulation of
E-
cadherin in different cell densities in the presence and absence of E6 protein. Our results suggest the role for post-translational regulation of surface
E-
cadherin by E6, when cells are at high density and in cell-to-cell contact. When cells are grown sparsely,
E-
cadherin was transcriptionally regulated by E6. We hypothesised that when cells were grown at high density, regulation of surface
E-
cadherin by HPV16 E6 occurred by affecting
E-
cadherin trafficking at the cell membrane. Analysis of
E-
cadherin endocytosis showed that there was reduced
E-
cadherin endocytosis in cells expressing E6. We observed up regulation of
E-
cadherin ubiquitination in E6 expressing cells, suggesting a role for the ubiquitination machinery in the E6-dependent reduction in surface
E-
cadherin.
Although there was no indication of E6 control over
E-
cadherin transcription in dense cultures, we did observe abnormal localisation of SNAI2
E-
cadherin gene repressor, in E6 expressing cells. Expression of E6 increased SNAI2 nuclear accumulation, indicating a potential function for SNAI2 in the nucleus that enables E6 control over
E-
cadherin. Upon further examination, we observed an increase in SNAI2 ubiquitination in E6 expressing cells, which suggests that similar to
E-
cadherin, SNAI2 is also regulated by E6 by ubiquitination. Treatment of cells with the proteosomal inhibitor MG132 revealed an inverse relationship between SNAI2 levels and its ubiquitination status in E6 cells, indicatinga novel degradation pathway that is important in E6 dependent SNAI2 regulation.
Here, we have shown that
E-
cadherin regulation by HPV16 E6 in dense HCT116 cells occurs at the post-translational level. Our overall data revealed a role of the ubiquitination pathway as a potential mechanism utilised by HPV 16 E6 to regulate surface
E-
cadherin. A similar ubiquitination pathway might also be employed by E6 to regulate SNAI2 protein expression. Although we have yet to determine the association between E6 dependent SNAI2 abnormalities and
E-
cadherin regulation, our findings suggest a contribution of protein ubiquitination in controlling
E-
cadherin and SNAI2 trafficking in the presence of HPV16 E6. These findings require further exploration to determine the…
Advisors/Committee Members: Hibma, Merilyn (advisor).
Subjects/Keywords: HPV16;
E6;
E-cadherin
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APA (6th Edition):
Yajid, . A. I. (n.d.). Human Papillomavirus Type 16 E6 Regulation Of Human Adhesion Protein, E-cadherin
. (Doctoral Dissertation). University of Otago. Retrieved from http://hdl.handle.net/10523/5853
Note: this citation may be lacking information needed for this citation format:
No year of publication.
Chicago Manual of Style (16th Edition):
Yajid, Aidy Irman. “Human Papillomavirus Type 16 E6 Regulation Of Human Adhesion Protein, E-cadherin
.” Doctoral Dissertation, University of Otago. Accessed January 19, 2021.
http://hdl.handle.net/10523/5853.
Note: this citation may be lacking information needed for this citation format:
No year of publication.
MLA Handbook (7th Edition):
Yajid, Aidy Irman. “Human Papillomavirus Type 16 E6 Regulation Of Human Adhesion Protein, E-cadherin
.” Web. 19 Jan 2021.
Note: this citation may be lacking information needed for this citation format:
No year of publication.
Vancouver:
Yajid AI. Human Papillomavirus Type 16 E6 Regulation Of Human Adhesion Protein, E-cadherin
. [Internet] [Doctoral dissertation]. University of Otago; [cited 2021 Jan 19].
Available from: http://hdl.handle.net/10523/5853.
Note: this citation may be lacking information needed for this citation format:
No year of publication.
Council of Science Editors:
Yajid AI. Human Papillomavirus Type 16 E6 Regulation Of Human Adhesion Protein, E-cadherin
. [Doctoral Dissertation]. University of Otago; Available from: http://hdl.handle.net/10523/5853
Note: this citation may be lacking information needed for this citation format:
No year of publication.
University of Georgia
18.
Uribe, Jacqueline.
Assessment of an E-cadherin BAC transgene for studies on anterior eye development.
Degree: 2014, University of Georgia
URL: http://hdl.handle.net/10724/30683
► E-Cadherin is part of a large family of Ca2+ dependent cell adhesion molecules that are fundamentally important for normal eye development. The use of BAC…
(more)
▼ E-Cadherin is part of a large family of Ca2+ dependent cell adhesion molecules that are fundamentally important for normal eye development. The use of BAC transgenic mice for gene expression mapping, highly depends on the accuracy of the
expression data obtained. In order to determine if GENSATs EGFP BAC transgene was faithfully replicating E-cadherin's expression pattern within the eye, I directly compared EGFP and E-cadherin expression in sections through the eye of transgenic embryos
at E10.5, E12.5, E17.5, P0, and adult mice. I show that this BAC transgene faithfully replicated E-cadherin expression in the developing eye at E10.5, E12.5, and E17.5. However, ectopic EGFP expression was observed in P0 and adult mice eyes. Together,
these findings suggest that the BAC transgene faithfully replicates E- cadherin expression only during embryonic development and not in P0 or adult mice eyes.
Subjects/Keywords: E-cadherin; cdh1; BAC transgene; eye; development; mouse; expression
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APA ·
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MLA ·
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CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Uribe, J. (2014). Assessment of an E-cadherin BAC transgene for studies on anterior eye development. (Thesis). University of Georgia. Retrieved from http://hdl.handle.net/10724/30683
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Uribe, Jacqueline. “Assessment of an E-cadherin BAC transgene for studies on anterior eye development.” 2014. Thesis, University of Georgia. Accessed January 19, 2021.
http://hdl.handle.net/10724/30683.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Uribe, Jacqueline. “Assessment of an E-cadherin BAC transgene for studies on anterior eye development.” 2014. Web. 19 Jan 2021.
Vancouver:
Uribe J. Assessment of an E-cadherin BAC transgene for studies on anterior eye development. [Internet] [Thesis]. University of Georgia; 2014. [cited 2021 Jan 19].
Available from: http://hdl.handle.net/10724/30683.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Uribe J. Assessment of an E-cadherin BAC transgene for studies on anterior eye development. [Thesis]. University of Georgia; 2014. Available from: http://hdl.handle.net/10724/30683
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
University of Ottawa
19.
Ooi, Sarah.
Expression Levels of E-cadherin in Breast Cancer Cells Alter Apoptotic Susceptibility and Facilitate Cancer Stem Cell Phenotypes in Response to Wnt Signalling
.
Degree: 2015, University of Ottawa
URL: http://hdl.handle.net/10393/32961
► It is well established that the Wnt pathway is associated with tumorigenesis in a wide range of human cancers, including a majority of breast cancers.…
(more)
▼ It is well established that the Wnt pathway is associated with tumorigenesis in a wide range of human cancers, including a majority of breast cancers. However, due to diverse roles of Wnt signalling, therapeutic targeting has not yielded consistent results and underlying mechanisms remain unclear. Here, I show that breast cancer cell lines with high E-cadherin expression are resistant to TCF4 inhibitors and develop cancer stem cell characteristics. Conversely, cells with low levels of E-cadherin are very susceptible to cell death with the same treatment. My results suggest that breast cancer cells in an epithelial-like state, but not mesenchymal-like state, will be more responsive to therapeutic targeting of the Wnt/TCF pathway. Importantly, E-cadherin high cells show robust Akt activation, whereas E-cadherin low cells do not. Thus, combinational inhibition of both Wnt and Akt signalling is needed to effectively target breast cancer cells in both the epithelial and mesenchymal states.
Subjects/Keywords: breast cancer;
E-cadherin;
cancer stem cells;
Wnt;
Akt
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APA ·
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APA (6th Edition):
Ooi, S. (2015). Expression Levels of E-cadherin in Breast Cancer Cells Alter Apoptotic Susceptibility and Facilitate Cancer Stem Cell Phenotypes in Response to Wnt Signalling
. (Thesis). University of Ottawa. Retrieved from http://hdl.handle.net/10393/32961
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Ooi, Sarah. “Expression Levels of E-cadherin in Breast Cancer Cells Alter Apoptotic Susceptibility and Facilitate Cancer Stem Cell Phenotypes in Response to Wnt Signalling
.” 2015. Thesis, University of Ottawa. Accessed January 19, 2021.
http://hdl.handle.net/10393/32961.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Ooi, Sarah. “Expression Levels of E-cadherin in Breast Cancer Cells Alter Apoptotic Susceptibility and Facilitate Cancer Stem Cell Phenotypes in Response to Wnt Signalling
.” 2015. Web. 19 Jan 2021.
Vancouver:
Ooi S. Expression Levels of E-cadherin in Breast Cancer Cells Alter Apoptotic Susceptibility and Facilitate Cancer Stem Cell Phenotypes in Response to Wnt Signalling
. [Internet] [Thesis]. University of Ottawa; 2015. [cited 2021 Jan 19].
Available from: http://hdl.handle.net/10393/32961.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Ooi S. Expression Levels of E-cadherin in Breast Cancer Cells Alter Apoptotic Susceptibility and Facilitate Cancer Stem Cell Phenotypes in Response to Wnt Signalling
. [Thesis]. University of Ottawa; 2015. Available from: http://hdl.handle.net/10393/32961
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
University of Toronto
20.
Shipstone, Arun.
Analysis of Alpha-catenin Mediated Intercellular Adhesion in Drosophila.
Degree: 2015, University of Toronto
URL: http://hdl.handle.net/1807/88582
► Dynamic linkage between the cadherin-catenin complex (CCC) and the actin cytoskeleton at Adherens Junctions is essential for cell-cell adhesion in epithelial cells. Alpha-catenin is a…
(more)
▼ Dynamic linkage between the cadherin-catenin complex (CCC) and the actin cytoskeleton at Adherens Junctions is essential for cell-cell adhesion in epithelial cells. Alpha-catenin is a core component of the CCC that is responsible for maintaining the linkage between the actin cytoskeleton and the CCC.
As part of my project, I generated an alpha-Catenin (alpha-Cat) RNAi line that was used to knockdown maternal alpha-Cat in Drosophila embryos. Knockdown of alpha-Cat in the female germline produced embryonic lethality that was characterized by severe defects throughout the embryo which suggests that the maternal contribution of alpha-Cat is indispensable for embryonic development.
I also investigated if alpha-catenin function is conserved among metazoans and Dictyostelium discoideum. I generated rescue constructs using mouse, zebrafish, worm and slime mold alpha-catenin proteins and attempted to rescue alpha-Cat1 mutant embryos. The results of my analysis suggest that alpha-catenin function is conserved among metazoans but not between Dictyostelium and metazoans.
M.Sc.
2018-03-09 00:00:00
Advisors/Committee Members: Tepass, Ulrich, Cell and Systems Biology.
Subjects/Keywords: alpha-catenin; Beta-catenin; catenin; cell adhesion; Drosophila; E-Cadherin; 0379
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APA ·
Chicago ·
MLA ·
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CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Shipstone, A. (2015). Analysis of Alpha-catenin Mediated Intercellular Adhesion in Drosophila. (Masters Thesis). University of Toronto. Retrieved from http://hdl.handle.net/1807/88582
Chicago Manual of Style (16th Edition):
Shipstone, Arun. “Analysis of Alpha-catenin Mediated Intercellular Adhesion in Drosophila.” 2015. Masters Thesis, University of Toronto. Accessed January 19, 2021.
http://hdl.handle.net/1807/88582.
MLA Handbook (7th Edition):
Shipstone, Arun. “Analysis of Alpha-catenin Mediated Intercellular Adhesion in Drosophila.” 2015. Web. 19 Jan 2021.
Vancouver:
Shipstone A. Analysis of Alpha-catenin Mediated Intercellular Adhesion in Drosophila. [Internet] [Masters thesis]. University of Toronto; 2015. [cited 2021 Jan 19].
Available from: http://hdl.handle.net/1807/88582.
Council of Science Editors:
Shipstone A. Analysis of Alpha-catenin Mediated Intercellular Adhesion in Drosophila. [Masters Thesis]. University of Toronto; 2015. Available from: http://hdl.handle.net/1807/88582
Freie Universität Berlin
21.
Redmer, Torben.
Deciphering the role of E-cadherin in pluripotency and reprogramming.
Degree: 2011, Freie Universität Berlin
URL: http://dx.doi.org/10.17169/refubium-13658
► During early embryogenesis the expression of cell adhesion molecules and the establishment of cell-cell contacts are crucial steps to ensure proper development of the embryo.…
(more)
▼ During early embryogenesis the expression of cell adhesion molecules and the
establishment of cell-cell contacts are crucial steps to ensure proper
development of the embryo. Especially expression of the molecule
E-
Cadherin, a
member of the
cadherin superfamily, is crucial for the formation of the
compacted morula, comprising an early stage of embryogenesis that forms the
blastocyst. The latter bears the inner cells mass (ICM), a group of
pluripotent cells, that forms all cells of the adult body. Cells of the ICM
can be used to establish embryonic stem cells (ESCs) as an in vitro system
that allows providing insights in these early differentiation processes.
Embryonic stem cells like cells of the ICM display high expression levels of
E-
Cadherin and of the pluripotency markers Oct4 and Nanog. In the present
work, the function of
E-
Cadherin in murine embryonic stem cells and during the
process of somatic cell reprogramming was analysed. It could been shown in a
shRNA mediated knock-down of
E-
Cadherin that its expression not only
determines the morphology of ESCs but is also linked to regulation of the
pluripotency genes Oct4 and Nanog. Further, cre/loxP mediated ablation of
E-
cadherin and beta-catenin expression followed by the reprogramming with four
viral factors Oct4, Sox2, Klf4 and c-Myc (OSKM) led to a strong reduction in
the number of induced pluripotent stem cell (iPS-cell) colonies. Therefore,
the establishment of the
E-
Cadherin/beta-Catenin complex is a crucial step in
the process that governs the conversion of fibroblasts to iPS-cells. Although
the link between
E-
Cadherin mediated cell adhesion and the regulation of Oct4
seems to be indirect, overexpression of
E-
cadherin in combination with SKM
surprisingly, led to the formation of stable ESKM-iPS clones. Cells of these
clones displayed endogenous expression of Oct4 and Nanog although exogenous
Oct4 was absent during the reprogramming process. Established ESKM-iPS cells
fulfilled all criteria tested so far, to establish their pluripotent state.
ESKM-iPS cells were able to undergo embryoid body mediated differentiation and
formed teratoma. The generation of these unconventional generated iPS cells
points out that pluripotency, beside transcription factors, is also defined by
the adhesive integrity of iPS and ES-cells. Especially
E-
Cadherin mediated
cell adhesion plays a crucial for the establishment and maintenance of the
pluripotent state.
Advisors/Committee Members: [email protected] (contact), [email protected] (contact), m (gender), Prof. Dr. Claus Scheidereit (firstReferee), Prof. Dr. Petra Knaus (furtherReferee).
Subjects/Keywords: E-Cadherin; Oct4; Pluripotency; 500 Naturwissenschaften und Mathematik::570 Biowissenschaften; Biologie
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APA (6th Edition):
Redmer, T. (2011). Deciphering the role of E-cadherin in pluripotency and reprogramming. (Thesis). Freie Universität Berlin. Retrieved from http://dx.doi.org/10.17169/refubium-13658
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Redmer, Torben. “Deciphering the role of E-cadherin in pluripotency and reprogramming.” 2011. Thesis, Freie Universität Berlin. Accessed January 19, 2021.
http://dx.doi.org/10.17169/refubium-13658.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Redmer, Torben. “Deciphering the role of E-cadherin in pluripotency and reprogramming.” 2011. Web. 19 Jan 2021.
Vancouver:
Redmer T. Deciphering the role of E-cadherin in pluripotency and reprogramming. [Internet] [Thesis]. Freie Universität Berlin; 2011. [cited 2021 Jan 19].
Available from: http://dx.doi.org/10.17169/refubium-13658.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Redmer T. Deciphering the role of E-cadherin in pluripotency and reprogramming. [Thesis]. Freie Universität Berlin; 2011. Available from: http://dx.doi.org/10.17169/refubium-13658
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
University of Melbourne
22.
Liu, David Shi Hao.
Therapeutic targeting of mutant p53 in oesophageal adenocarcinoma.
Degree: 2017, University of Melbourne
URL: http://hdl.handle.net/11343/130108
► Oesophageal adenocarcinoma (OAC) is a lethal disease with a rapidly rising incidence. The standard of care for patients with early stage OAC is surgery combined…
(more)
▼ Oesophageal adenocarcinoma (OAC) is a lethal disease with a rapidly rising incidence. The standard of care for patients with early stage OAC is surgery combined with either neoadjuvant chemo-radiotherapy or perioperative chemotherapy. However, over 70% of patients present with unresectable or metastatic disease. In this setting, their treatment options are significantly limited, and their overall clinical outcome is exceedingly poor, with a median survival of under 12 months. Therefore, safe and effective therapies for patients with OAC are an urgent and unmet medical need.
Mutations in the tumour suppressor gene TP53 are by far the most common genetic alteration in OAC. This phenomenon occurs early in oesophageal carcinogenesis and often results in stabilisation of mutant p53 (mut-p53) protein. The loss of wild-type p53 (wt-p53) tumour suppressor activity together with the acquisition of mut-p53 oncogenic gain-of-function, likely drives tumour progression resulting in poor patient survival. Mut-p53 is thus a potential therapeutic target in OAC. In particular, restoring wild-type tumour suppressor activity to mut-p53 should lead to cancer-specific cell death.
APR-246, the prototypical mut-p53 reactivator, has been shown to refold mut-p53 protein into wild-type conformation, restoring wild-type activity leading to transcriptional upregulation of wt-p53 target genes. This drug has proven preclinical efficacy and was recently evaluated in early phase clinical trials. In patients with haematological, prostatic and ovarian malignancies, APR-246 was shown to be well tolerated whilst achieving p53-dependent therapeutic effects. As a result, this drug is currently being further studied in a randomised phase II trial for patients with high grade serous ovarian cancer. Given the prevalence of p53 mutations in OAC (>70%), this thesis firstly investigated the anti-tumour activity of APR-246 in preclinical models of OAC.
In cell line and patient derived xenografts of OAC, APR-246 demonstrated significant therapeutic effect. Treatment with APR-246 up-regulated the expression of canonical wt-p53 target genes, inhibited clonogenic survival and induced cell cycle arrest as well as apoptosis in mut-p53 OAC cells. This anti-tumour activity was observed in cancer cells harbouring a wide range of p53 mutants. Interestingly, endogenous levels of mut-p53 protein closely correlated with cellular sensitivity to APR-246. From a translational perspective, APR-246 synergistically enhanced the cytotoxicity of conventional chemotherapies including cisplatin, 5-fluorouracil and epirubicin. Moreover, it also overcame intrinsic chemoresistance to these agents. Importantly, based on genetic knockdown and knockout studies of mut-p53, this thesis uncovered significant p53-independent effects of APR-246.
Following in-depth analysis into the p53-independent mechanisms of action of APR-246, this thesis found that APR-246 depleted intracellular glutathione and triggered lipid peroxidative cell death. Extending this, the cellular…
Subjects/Keywords: Oesophageal cancer; Cancer therapies; TP53; Animal models; E-cadherin; Xenografts
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APA (6th Edition):
Liu, D. S. H. (2017). Therapeutic targeting of mutant p53 in oesophageal adenocarcinoma. (Doctoral Dissertation). University of Melbourne. Retrieved from http://hdl.handle.net/11343/130108
Chicago Manual of Style (16th Edition):
Liu, David Shi Hao. “Therapeutic targeting of mutant p53 in oesophageal adenocarcinoma.” 2017. Doctoral Dissertation, University of Melbourne. Accessed January 19, 2021.
http://hdl.handle.net/11343/130108.
MLA Handbook (7th Edition):
Liu, David Shi Hao. “Therapeutic targeting of mutant p53 in oesophageal adenocarcinoma.” 2017. Web. 19 Jan 2021.
Vancouver:
Liu DSH. Therapeutic targeting of mutant p53 in oesophageal adenocarcinoma. [Internet] [Doctoral dissertation]. University of Melbourne; 2017. [cited 2021 Jan 19].
Available from: http://hdl.handle.net/11343/130108.
Council of Science Editors:
Liu DSH. Therapeutic targeting of mutant p53 in oesophageal adenocarcinoma. [Doctoral Dissertation]. University of Melbourne; 2017. Available from: http://hdl.handle.net/11343/130108
Aristotle University Of Thessaloniki (AUTH); Αριστοτέλειο Πανεπιστήμιο Θεσσαλονίκης (ΑΠΘ)
23.
Konstantara, Athina.
Μοριακή μελέτη της οδού μεταγωγής σήματος WNT στον καρκίνο του γαστρεντερικού συστήματος.
Degree: 2014, Aristotle University Of Thessaloniki (AUTH); Αριστοτέλειο Πανεπιστήμιο Θεσσαλονίκης (ΑΠΘ)
URL: http://hdl.handle.net/10442/hedi/36894
► INTRODUCTION: Gastric and Colorectal cancer remain a major cause of mortality, despite the implementation of screening strategies and early detection. Although clinicopathological characteristics seem to…
(more)
▼ INTRODUCTION: Gastric and Colorectal cancer remain a major cause of mortality, despite the implementation of screening strategies and early detection. Although clinicopathological characteristics seem to distinguish a subset of patients that are at high risk of relapse, the need for molecular markers that would help to discriminate the high-risk population is still unmet.AIM: The aim of that study is to explore the differential expression of the WNT members and their effectors according to their location in the tumor, identify their prognostic role in a cohort of non-metastatic surgically treated patients and reveal correlations with the various clinicopathological parameters.MATERIALS-METHODS: This is a study based on a series of fully characterized patients with colorectal cancer as well a second cohort of patients with gastric cancer. Immunohistochemical expression of nuclear cyclin D1, membranous E-cadherin and P-cadherin, membranous and nuclear β-catenin in the invasive front (IF), the tumor center (TC), as well as their mean, were assessed in 106 paraffin-embedded tissue samples for the colorectal cancer cohort and 36 for the gastric cohort. Adenomatous Polyposis Coli (APC), Axin2 (AXIN2), cyclin D1 (CCND1), Matrix Metalloproteinase 7 (MMP7), Secreted Frizzled Related Protein (SFRP) 1,2 and 4 and WNT5A were evaluated by RT-PCR. RESULTS: The study series included 106 patients with colorectal cancer, 70 with colonic and 36 with rectal cancer and 32 patients with gastric cancer. Immunohistochemical expression of the different markers were assessed in the tumor center (TC) and invasive front (IF). Membranous β-catenin expression was statistically reduced in the IF. Cyclin D1 was reduced in tumors arising closer to the rectum. We also observed that reduced nuclear expression of cyclin D1 in the IF was associated with lymphatic, venous and perineural invasion. Loss of membranous β-catenin in the TC was more common among N2 tumors. Higher SFRP4 mRNA was associated with T3 stage. In univariate analysis, membranous expression of β-catenin in TC and IF, and their mean, was associated with longer disease-free survival (DFS). In multivariate analysis, tumor stage and mean β-catenin expression were prognostic for longer DFS (hazard ratio=0.33; p=0.01). Β-catenin expression in the IF remained significant when the mean expression was not included in the multivariate analysis (hazard ratio=0.41; p=0.028) In case of gastric cancer, membranous expression of P-cadherin, in univariate analysis, was associated with longer survival.CONCLUSION: Underexpression of membranous β-catenin mean as well as expression in the IF seems to identify a higher risk subset of patients surgically treated for colorectal cancer with shorter disease-free survival (DFS). As far as gastric cancer is concerned, results showed that overexpression of membranous P-cadherin was associated with better survival. Further evaluation in a larger cohort is mandatory to validate this results.
ΕΙΣΑΓΩΓΗ: Ο γαστρικός και ο ορθοκολικός καρκίνος παραμένουν από τις…
Subjects/Keywords: β-κατενίνη; Ε-κατχερίνη; Wnt; b-catenin; E-cadherin; Pcadherin
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APA (6th Edition):
Konstantara, A. (2014). Μοριακή μελέτη της οδού μεταγωγής σήματος WNT στον καρκίνο του γαστρεντερικού συστήματος. (Thesis). Aristotle University Of Thessaloniki (AUTH); Αριστοτέλειο Πανεπιστήμιο Θεσσαλονίκης (ΑΠΘ). Retrieved from http://hdl.handle.net/10442/hedi/36894
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Konstantara, Athina. “Μοριακή μελέτη της οδού μεταγωγής σήματος WNT στον καρκίνο του γαστρεντερικού συστήματος.” 2014. Thesis, Aristotle University Of Thessaloniki (AUTH); Αριστοτέλειο Πανεπιστήμιο Θεσσαλονίκης (ΑΠΘ). Accessed January 19, 2021.
http://hdl.handle.net/10442/hedi/36894.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Konstantara, Athina. “Μοριακή μελέτη της οδού μεταγωγής σήματος WNT στον καρκίνο του γαστρεντερικού συστήματος.” 2014. Web. 19 Jan 2021.
Vancouver:
Konstantara A. Μοριακή μελέτη της οδού μεταγωγής σήματος WNT στον καρκίνο του γαστρεντερικού συστήματος. [Internet] [Thesis]. Aristotle University Of Thessaloniki (AUTH); Αριστοτέλειο Πανεπιστήμιο Θεσσαλονίκης (ΑΠΘ); 2014. [cited 2021 Jan 19].
Available from: http://hdl.handle.net/10442/hedi/36894.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Konstantara A. Μοριακή μελέτη της οδού μεταγωγής σήματος WNT στον καρκίνο του γαστρεντερικού συστήματος. [Thesis]. Aristotle University Of Thessaloniki (AUTH); Αριστοτέλειο Πανεπιστήμιο Θεσσαλονίκης (ΑΠΘ); 2014. Available from: http://hdl.handle.net/10442/hedi/36894
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
University of Pennsylvania
24.
Till, Jacob Edward.
A New Mouse Model Of Metastatic Gastric Cancer And E-Cadherin Primary Tumor Suppression.
Degree: 2016, University of Pennsylvania
URL: https://repository.upenn.edu/edissertations/3059
► Gastric cancer is the fifth most common cancer and the third leading cause of cancer death worldwide. The majority of patients with gastric cancer are…
(more)
▼ Gastric cancer is the fifth most common cancer and the third leading cause of cancer death worldwide. The majority of patients with gastric cancer are diagnosed with disseminated disease and even patients diagnosed with early stage disease have high rates
of recurrence. The utility of current mouse models of gastric cancer is limited by slow development of gastric tumors and lack of metastasis. Here I describe a new mouse model of gastric cancer driven by p53 loss, Cdh1 loss, and oncogenic Kras expression in
gastric parietal cells (referred to as ACKPY mice). I generated these mice to investigate the contribution of oncogenic Kras to the progression of gastric cancer given the high rate of mutation and amplification of the RTK/Ras pathway identified in gastric cancer
patients. These mice develop mixed-type gastric adenocarcinomas with metastases to lymph nodes, lung, and liver. Oncogenic Kras and loss of Trp53 is sufficient to drive rapid carcinogenesis in a variety of models. Therefore, I tested if loss of E-cadherin was
necessary for the onset of gastric adenocarcinoma in gastric parietal cells by generating ACKPY mice with one or two alleles of wild-type Cdh1 (E-cadherin). E-cadherin expression significantly increased survival and the limited number of mice with gastric
tumors have tumors that were focal in nature, suggesting an additional event was necessary for gastric tumorigenesis. Loss of E-cadherin expression was observed in some of these tumors, suggesting that its loss may be necessary for gastric tumorigenesis in this model. I show that loss of E-cadherin in our model increases β-catenin signaling and that inhibition of β-catenin signaling prolonged survival of ACKPY mice. Microarray data comparing gene expression in stomachs harvested from Cdh1fl/fl and Cdh1fl/+ mice showed a correlation between E-cadherin loss and upregulation of oncogenic Kras signaling. Gene sets regulated by each of the main Kras effector pathways were overrepresented in our microarray data. Examination of ERK phosphorylation revealed that
E-cadherin likely does not regulate MAPK activity in our model. The upregulation of oncogenic Kras target genes that result from the loss of E-cadherin may alternatively be explained by E-cadherin regulation of other Kras effector pathways.
Subjects/Keywords: CDH1; E-Cadherin; Gastric Cancer; KRAS; Mouse Model; Oncology
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APA (6th Edition):
Till, J. E. (2016). A New Mouse Model Of Metastatic Gastric Cancer And E-Cadherin Primary Tumor Suppression. (Thesis). University of Pennsylvania. Retrieved from https://repository.upenn.edu/edissertations/3059
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Till, Jacob Edward. “A New Mouse Model Of Metastatic Gastric Cancer And E-Cadherin Primary Tumor Suppression.” 2016. Thesis, University of Pennsylvania. Accessed January 19, 2021.
https://repository.upenn.edu/edissertations/3059.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Till, Jacob Edward. “A New Mouse Model Of Metastatic Gastric Cancer And E-Cadherin Primary Tumor Suppression.” 2016. Web. 19 Jan 2021.
Vancouver:
Till JE. A New Mouse Model Of Metastatic Gastric Cancer And E-Cadherin Primary Tumor Suppression. [Internet] [Thesis]. University of Pennsylvania; 2016. [cited 2021 Jan 19].
Available from: https://repository.upenn.edu/edissertations/3059.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Till JE. A New Mouse Model Of Metastatic Gastric Cancer And E-Cadherin Primary Tumor Suppression. [Thesis]. University of Pennsylvania; 2016. Available from: https://repository.upenn.edu/edissertations/3059
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
25.
Teixeira, Tarso Felipe.
Melanomas melânicos e amelânicos da cavidade bucal de cães: aspectos epidemiológicos, morfológicos e moleculares.
Degree: PhD, Patologia Experimental e Comparada, 2011, University of São Paulo
URL: http://www.teses.usp.br/teses/disponiveis/10/10133/tde-19102012-082041/
;
► Melanoma é uma neoplasia maligna com comportamento agressivo considerado o câncer mais comum da cavidade bucal de cães. Ele pode ser classificado quanto a morfologia…
(more)
▼ Melanoma é uma neoplasia maligna com comportamento agressivo considerado o câncer mais comum da cavidade bucal de cães. Ele pode ser classificado quanto a morfologia celular em epitelióide, fusiforme e misto ou quanto ao fenótipo: melânico ou amelânico. Estudos têm sugerido que os melanomas amelânicos são mais agressivos. O objetivo deste estudo foi avaliar o comportamento dos melanomas da cavidade bucal dos cães, quantificando a expressão das Cx26 e 43, caderina-E, MMPs 2 e 9 e proliferação celular. Para tanto foram coletados 25 melanomas provenientes de cães atendidos no HOVET FMVZ-USP (16 melânicos e 9 amelânicos). Após a cirurgia os animais foram acompanhados até a morte, sendo que 5 animais foram eutanasiados (2 antes da cirurgia e 3 após o procedimento cirúrgico, devido ao sofrimento físico). Os tumores eram diagnosticados através do histopatológico e classificados de acordo com OMS (1998). Para confirmação dos melanomas amelânicos foi utilizado à técnica de imuno-histoquímica com o perfil de anticorpos pré-estabelecidos. A proliferação celular foi quantificada através do uso de PCNA, índice apoptótico e caspase-3. O comportamento tumoral foi avaliado através da técnica de imuno-histoquímica para caderina-E e MMPs 2 e 9. E a expressão das Cxs foram avaliadas através da imunofluorescência e western blot. Cães com melanma amelânico apresentaram menor sobrevida, com aumento do número de metástase, fraca marcação para caderina-E e alta intensidade para as MMPs 2 e 9, aumento de células positivas para PCNA e índice mitótico, e diminuição da caspase-3, não havendo diferença significante quanto aos tipos histotógicos. Houve diminuição de expressão das Cxs entre os amelânicos, no entanto, aumento da síntese do gene de CX 26 entre o mesmo grupo, o que se verificou através do PCR em Tempo Real. Nossos achados sugerem que os melanomas da cavidade bucal de cães apresentam um comportamento mais agressivo
Melanoma is a malignant neoplasm with aggressive behavior considered the most common cancer of the buccal cavity in dogs. It can be classified as cell morphology in epithelioid, spindle and mixed or on the phenotype, in melanotic or amelanotic. Studies have suggested that amelanotic melanomas are more aggressive. The aim of this study was to evaluate the behavior of melanoma of the buccal cavity of dogs, quantifying the expression of Connexins 26 and 43, E-cadherin, MMPs 2 and 9 and cell proliferation. For both melanomas were collected from 25 dogs attended at HOVET FMVZ (USP) (16 melanotic and 9 amelanotic melanomas). After the surgery, the animals were followed until death, so 5 animals were euthanized (2 before surgery and 3 after surgery, due to physical suffering). The tumors were diagnosed by histopathology and classified according to WHO (1998). For confirmation of amelanotic melanomas it was used the technique of immune-histochemistry with the antibody profile pre-established. Cell proliferation was quantified by using PCNA, apoptotic index and caspase-3. The tumor behavior was evaluated…
Advisors/Committee Members: Dagli, Maria Lucia Zaidan.
Subjects/Keywords: Amelânico; Amelanotic; Caderina-E; Conexinas; Connexins; E-Cadherin; Melanoma; Melanoma; Metalloproteinases; Metaloproteinases
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APA ·
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APA (6th Edition):
Teixeira, T. F. (2011). Melanomas melânicos e amelânicos da cavidade bucal de cães: aspectos epidemiológicos, morfológicos e moleculares. (Doctoral Dissertation). University of São Paulo. Retrieved from http://www.teses.usp.br/teses/disponiveis/10/10133/tde-19102012-082041/ ;
Chicago Manual of Style (16th Edition):
Teixeira, Tarso Felipe. “Melanomas melânicos e amelânicos da cavidade bucal de cães: aspectos epidemiológicos, morfológicos e moleculares.” 2011. Doctoral Dissertation, University of São Paulo. Accessed January 19, 2021.
http://www.teses.usp.br/teses/disponiveis/10/10133/tde-19102012-082041/ ;.
MLA Handbook (7th Edition):
Teixeira, Tarso Felipe. “Melanomas melânicos e amelânicos da cavidade bucal de cães: aspectos epidemiológicos, morfológicos e moleculares.” 2011. Web. 19 Jan 2021.
Vancouver:
Teixeira TF. Melanomas melânicos e amelânicos da cavidade bucal de cães: aspectos epidemiológicos, morfológicos e moleculares. [Internet] [Doctoral dissertation]. University of São Paulo; 2011. [cited 2021 Jan 19].
Available from: http://www.teses.usp.br/teses/disponiveis/10/10133/tde-19102012-082041/ ;.
Council of Science Editors:
Teixeira TF. Melanomas melânicos e amelânicos da cavidade bucal de cães: aspectos epidemiológicos, morfológicos e moleculares. [Doctoral Dissertation]. University of São Paulo; 2011. Available from: http://www.teses.usp.br/teses/disponiveis/10/10133/tde-19102012-082041/ ;
26.
Poppe, Ana Carolina Machado.
Avaliação de marcadores relacionados à transição epitélio-mesênquima na endometriose pélvica.
Degree: Mestrado, Obstetrícia e Ginecologia, 2013, University of São Paulo
URL: http://www.teses.usp.br/teses/disponiveis/5/5139/tde-20022014-092016/
;
► Introdução: A endometriose é uma doença ginecológica comum caracterizada pela presença de estroma e/ou glândula endometrial fora da cavidade uterina, e que não possui sua…
(more)
▼ Introdução: A endometriose é uma doença ginecológica comum caracterizada pela presença de estroma e/ou glândula endometrial fora da cavidade uterina, e que não possui sua etiopatogenia bem estabelecida. A transição epitélio-mesênquima (TEM) é um processo que consiste em uma série de mudanças no fenótipo de células epiteliais que fazem com que estas células assumam características de células mesenquimais. Assim como observado na TEM, as células endometriais no contexto da endometriose apresentam capacidade migratória, invasibilidade e elevada resistência à apoptose. As moléculas de adesão têm adquirido crescente relevância na TEM, pois relacionam-se à perda de adesão célula-célula com o aumento da invasão e metástase. O objetivo deste estudo foi investigar a expressão de marcadores relacionados com a TEM na endometriose superficial, ovariana e profunda. Pacientes e Métodos: Foram selecionadas 103 mulheres que preenchiam os critérios de inclusão estabelecidos, constituindo 2 grupos de estudo independentes entre si: 18 mulheres com endometriose peritoneal, ovariana e profunda concomitantes; 85 mulheres com endometriose ovariana e/ou profunda, dividido em 44 mulheres com endometriose ovariana e 41 com endometriose intestinal. Através de reações de imunoistoquímica, a expressão proteica dos marcadores e-caderina, n-caderina, betacatenina, receptor de estrogênio e receptor de progesterona foram avaliados nos tecidos de interesse em cada grupo de estudo. Além dos locais de doença, as mulheres foram avaliadas quanto à relação com a fase do ciclo e à classificação histológica da doença. Resultados: As lesões de endometriose de ovário mostraram uma menor expressão de n-caderina em comparação às lesões de intestino e peritônio (p=0,032). O receptor de estrogênio e receptor de progesterona se mostraram significativamente menos expressos no componente epitelial da doença de ovário do que no epitélio da endometriose de peritônio e intestino (p=0,002; p=0,48). A expressão da n-caderina apresentou uma correlação direta com a expressão do receptor de estrogênio no estroma da endometriose de intestino (p=0,036). Conclusão: Estes resultados sugerem que a transição epitélio-mesênquima esteja envolvida na etiopatogenia da endometriose, demonstrando que a doença de ovário se comporta de maneira diferente da doença superficial e da doença infiltrativa profunda, sendo a n-caderina um importante fator envolvido neste processo possivelmente influenciada pela ação do estrogênio
Background: Endometriosis is a common gynecological disease defined as the presence of ectopic endometrial glands and stroma outside the uterine cavity, and its pathogenesis is not well established. The epithelial to mesenchymal transition (EMT) is a process consisting of a series of changes in the phenotype of epithelial cells that make these cells assume the characteristics of mesenchymal cells. As observed in the EMT, endometrial cells in the context of endometriosis have the capacity of migration, invasiveness and high resistance to apoptosis. . The adhesion…
Advisors/Committee Members: Abrão, Mauricio Simões.
Subjects/Keywords: beta-catenin; Beta-catenina; E-caderinas; E-cadherin; Endometriose; Endometriosis; Epithelial-mesenchymal transition; Estrogen receptor; N-caderinas; N-cadherin; Progesterone receptor; Receptores de progesterona; Receptores estrogênicos; Transição epitélial-mesenquimal
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APA (6th Edition):
Poppe, A. C. M. (2013). Avaliação de marcadores relacionados à transição epitélio-mesênquima na endometriose pélvica. (Masters Thesis). University of São Paulo. Retrieved from http://www.teses.usp.br/teses/disponiveis/5/5139/tde-20022014-092016/ ;
Chicago Manual of Style (16th Edition):
Poppe, Ana Carolina Machado. “Avaliação de marcadores relacionados à transição epitélio-mesênquima na endometriose pélvica.” 2013. Masters Thesis, University of São Paulo. Accessed January 19, 2021.
http://www.teses.usp.br/teses/disponiveis/5/5139/tde-20022014-092016/ ;.
MLA Handbook (7th Edition):
Poppe, Ana Carolina Machado. “Avaliação de marcadores relacionados à transição epitélio-mesênquima na endometriose pélvica.” 2013. Web. 19 Jan 2021.
Vancouver:
Poppe ACM. Avaliação de marcadores relacionados à transição epitélio-mesênquima na endometriose pélvica. [Internet] [Masters thesis]. University of São Paulo; 2013. [cited 2021 Jan 19].
Available from: http://www.teses.usp.br/teses/disponiveis/5/5139/tde-20022014-092016/ ;.
Council of Science Editors:
Poppe ACM. Avaliação de marcadores relacionados à transição epitélio-mesênquima na endometriose pélvica. [Masters Thesis]. University of São Paulo; 2013. Available from: http://www.teses.usp.br/teses/disponiveis/5/5139/tde-20022014-092016/ ;
NSYSU
27.
Pan, Lin-Lin.
Evaluation of E-cadherin gene expression in cervical carcinomas.
Degree: Master, Biological Sciences, 2003, NSYSU
URL: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0828103-093840
► Epithelial adhesion molecule, E-cadherin plays important role in maintaining structural integrity of epithelial tissue. Altered expression of E-cadherin might result in the loss of contact…
(more)
▼ Epithelial adhesion molecule,
E-
cadherin plays important role in maintaining structural integrity of epithelial tissue. Altered expression of
E-
cadherin might result in the loss of contact inhibition growth property, abnormal cell growth and differentiation, hence the oncogenic transformation.
To explore the role of
E-
cadherin in the tumor progression, we have investigate the expression pattern of
E-
cadherin in invasive cervical carcinomas. 77 paraffin embedded specimen with FIGO staging Iaï¼N=15ï¼, Ibï¼N=19ï¼, Ib metaï¼N=13ï¼ IIaï¼N=17ï¼, IIbï¼N=13ï¼were included in immunohistochemical study, 18 surgical removed tumor tissues of Ib stage and its normal counter parts were used for semi-quantitative RT-PCR analysis. The results indicated that no significant correlation between
E-
cadherin expression level and tumor metasis, patient prognosis. However,
E-
cadherin immunostainimg intensity was significanty inverse correlated with tumor sizeï¼p < 0.001ï¼. Notably, loss of membranes
E-
cadherin expression might be a significant factor that correlated with tumor metasisï¼p = 0.001,< 0.005ï¼.
Advisors/Committee Members: none (chair), none (chair), none (committee member).
Subjects/Keywords: E-cadherin; cervical carcinomas; immunohistochemistry; metasis
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APA (6th Edition):
Pan, L. (2003). Evaluation of E-cadherin gene expression in cervical carcinomas. (Thesis). NSYSU. Retrieved from http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0828103-093840
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Pan, Lin-Lin. “Evaluation of E-cadherin gene expression in cervical carcinomas.” 2003. Thesis, NSYSU. Accessed January 19, 2021.
http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0828103-093840.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Pan, Lin-Lin. “Evaluation of E-cadherin gene expression in cervical carcinomas.” 2003. Web. 19 Jan 2021.
Vancouver:
Pan L. Evaluation of E-cadherin gene expression in cervical carcinomas. [Internet] [Thesis]. NSYSU; 2003. [cited 2021 Jan 19].
Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0828103-093840.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Pan L. Evaluation of E-cadherin gene expression in cervical carcinomas. [Thesis]. NSYSU; 2003. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0828103-093840
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
NSYSU
28.
Kung, Mei-Lang.
Investigation on the Mechanisms of Hepatoma-Derived Growth Factor-Mediated Cell Migration and Epithelial-Mesenchymal Transition.
Degree: PhD, Biological Sciences, 2012, NSYSU
URL: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0804112-214405
► In this study, we investigated the mechanisms of HDGF on cell migration in non-transformed NIH/3T3 cells. HDGF promoted the migration and the formation of dorsal…
(more)
▼ In this study, we investigated the mechanisms of HDGF on cell migration in non-transformed NIH/3T3 cells. HDGF promoted the migration and the formation of dorsal ruffles and podosome rosettes. Besides, HDGF supply increased the PI3K expression, Akt phosphorylation and PTEN phosphorylation as well as stimulated the RhoA, Rac1, and Cdc42 activities. Furthermore, Adenoviral gene transfer of PTEN attenuated migration and PI3K/Akt/Rho GTPases signaling in HDGF-overexpressing transfectants. Pharmaceutical intervention using the PI3K inhibitor, LY294002, potently reversed HDGF-stimulated cell migration, dorsal ruffles formation and podosome formation as well as the RhoA, Rac1, and Cdc42 activities. Thus, HDGF elicits the activation of PI3K/Akt /Rho GTPases signaling cascade and promotes cytoskeleton remodeling to stimulate cellular migration. Moreover, we investigate the expression profile of HDGF during breast carcinogenesis. Immunohistochemical studies revealed elevated HDGF expression in human breast cancer. Nuclear HDGF labelling index was positively correlated with tumour grade, stage and proliferation index, but negatively correlated with survival rate in breast cancer patients. Our data also showed that HDGF over-expression was associated with lymph node metastasis and represented an independent prognostic factor for tumor recurrence. Furthermore, Immunoblot study revealed that elevated HDGF expression significantly higher in breast cancer cells (MDA-MB-231 cells) than that in non-transformed breast cells (MCF-7 cells). Consistently, higher invasive potency and colony formation also observed in MDA-MB-231 cells than in MCF-7 cells. Adenovirus-mediated HDGF over-expression and exogenous HDGF treatment stimulated the invasiveness and colony formation as well as
E-
cadherin down-regulation and Vimentin up-regulation. Conversely, either HDGF knockdown by RNA interference, HDGF antibody neutralization or BITC-induced EMT suppression in MDA-MB-231 cells attenuated the malignant behavior and elicited EMT reversal by enhancing
E-
cadherin expression while depleting Vimentin expression.
In summary, HDGF elicits the activation of PI3K/Akt/Rho GTPases signaling cascade, thereby promoting cytoskeleton remodeling to stimulate cellular migration. Moreover, the formation of podosome rosettes is correlated with cell invasion, the podosome-stimulating capability of HDGF is consistent with HDGF regulates the metastasis of breast cancer through modulating of epithelial-mesenchymal transition. Therefore, our results provide not only novel insights into the role of the HDGF in cell migration and tumor metastasis, but also validate a novel prognostic indicator for breast cancer.
Key words: Hepatoma-derived growth factor, PI3K, Akt, epithelal-mesenchemal transition,
E-
cadherin, Vimentin
Advisors/Committee Members: Ming-Hong Tai (committee member), Yi-Ren Hong (chair), Jong-Kang Liu (committee member), Tsung-Hui Hu (chair), Hoi-Hung Chan (chair).
Subjects/Keywords: E-cadherin; PI3K; Vimentin; Akt; Hepatoma-derived growth factor; epithelal-mesenchemal transition
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APA ·
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APA (6th Edition):
Kung, M. (2012). Investigation on the Mechanisms of Hepatoma-Derived Growth Factor-Mediated Cell Migration and Epithelial-Mesenchymal Transition. (Doctoral Dissertation). NSYSU. Retrieved from http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0804112-214405
Chicago Manual of Style (16th Edition):
Kung, Mei-Lang. “Investigation on the Mechanisms of Hepatoma-Derived Growth Factor-Mediated Cell Migration and Epithelial-Mesenchymal Transition.” 2012. Doctoral Dissertation, NSYSU. Accessed January 19, 2021.
http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0804112-214405.
MLA Handbook (7th Edition):
Kung, Mei-Lang. “Investigation on the Mechanisms of Hepatoma-Derived Growth Factor-Mediated Cell Migration and Epithelial-Mesenchymal Transition.” 2012. Web. 19 Jan 2021.
Vancouver:
Kung M. Investigation on the Mechanisms of Hepatoma-Derived Growth Factor-Mediated Cell Migration and Epithelial-Mesenchymal Transition. [Internet] [Doctoral dissertation]. NSYSU; 2012. [cited 2021 Jan 19].
Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0804112-214405.
Council of Science Editors:
Kung M. Investigation on the Mechanisms of Hepatoma-Derived Growth Factor-Mediated Cell Migration and Epithelial-Mesenchymal Transition. [Doctoral Dissertation]. NSYSU; 2012. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0804112-214405
Universidade do Rio Grande do Sul
29.
Cadore, Ermani.
A expressão das claudinas 1, 3, 4, 7 e E-caderina em uma série de tumores de mama triplo-negativos.
Degree: 2012, Universidade do Rio Grande do Sul
URL: http://hdl.handle.net/10183/39662
► INTRODUÇÃO: O câncer de mama é uma importante causa de morbimortalidade, é conhecido por ser uma doença heterogênea. A caracterização clínica e molecular de seus…
(more)
▼ INTRODUÇÃO: O câncer de mama é uma importante causa de morbimortalidade, é conhecido por ser uma doença heterogênea. A caracterização clínica e molecular de seus subtipos é fundamental para nortear o prognóstico e o tratamento dessas pacientes. Novos estudos são necessários na melhor caracterização dos tumores triplo-negativos. O estudo da expressão das claudinas pode auxiliar na caracterização desses tumores. OBJETIVO: Investigar a associação da expressão das claudinas 1, 3, 4 e 7 e E-caderina com variáveis clínico-patológicas e fatores prognósticos, em uma série de tumores de mama triplo-negativos (RE-, RP- e HER2-). MÉTODOS: 80 tumores triplo-negativos foram analisados por imunoistoquímica automatizada para as claudinas 1, 3, 4, 7 e E-caderina. A expressão imunoistoquímica foi avaliada pelo escore H (intensidade multiplicada pela porcentagem de marcação). Foram avaliadas as associações entre características clínico-patólogicas e o escore H. Para a avaliação prognóstica das pacientes, curvas de Kaplan-Meier foram construídas a partir dos dados de seguimento das pacientes e do escore H. RESULTADOS: Foi encontrada associação significativa entre o alto escore H da CLDN-1 (HCLDN-1) e pacientes mais idosas e com a presença de necrose, alto escore H da E-caderina (HE-CAD) em pacientes mais jovens e baixo escore H da CLDN-7 (HCLDN-7) e Ki67 positivo. Além disso, pacientes com elevado HCLDN-1 tiveram menor sobrevida geral. Por outro lado, o elevado HCLDN-3 apresentou uma tendência à associação com maior sobrevida geral e sobrevida livre de doença. CONCLUSÕES: A expressão diferencial das claudinas e E-caderina podem auxiliar na caracterização clinico-patológica dos tumores triplo-negativos. Além disso, as claudinas 1 e 3 parecem ser fatores prognósticos para esses tumores.
INTRODUCTION: Breast cancer is a major cause of morbidity and mortality, is known to be a heterogeneous disease. The clinical and molecular characterization of its subtypes is critical to guide the prognosis and treatment of these patients. Further studies are needed for the best characterization of triple-negative tumors. The study of the expression of claudinas can aid in the characterization of these tumors. OBJECTIVE: To investigate the association of expression of claudinas 1, 3, 4 and 7 and E-cadherin with clinicopathological variables and prognosis in a series of triple-negative breast cancers (ER-, PR- and HER2-). METHODS: 80 triple negative tumors were analyzed by automated immunohistochemistry for the claudins 1, 3, 4, 7 and E-cadherin. The immunohistochemical expression was assessed by H-Score (intensity multiplied by the percentage of staining). We evaluated the associations between clinicopathological characteristics and H-Score. For the prognostic assessment of patients, Kaplan-Meier curves were constructed from the follow-up data of patients and H-Score. RESULTS: We found a significant association between high H-Score of CLDN-1 (HCLDN-1) and older patients and the presence of necrosis, high H-Score of E-cadherin (H-CAD) in younger…
Advisors/Committee Members: Graudenz, Márcia Silveira.
Subjects/Keywords: Breast cancer; Epidemiologia; Immunohistochemical markers; Neoplasias da mama; Claudins; Claudinas; Caderinas; E-cadherin; Triple-negative
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APA ·
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APA (6th Edition):
Cadore, E. (2012). A expressão das claudinas 1, 3, 4, 7 e E-caderina em uma série de tumores de mama triplo-negativos. (Thesis). Universidade do Rio Grande do Sul. Retrieved from http://hdl.handle.net/10183/39662
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Cadore, Ermani. “A expressão das claudinas 1, 3, 4, 7 e E-caderina em uma série de tumores de mama triplo-negativos.” 2012. Thesis, Universidade do Rio Grande do Sul. Accessed January 19, 2021.
http://hdl.handle.net/10183/39662.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Cadore, Ermani. “A expressão das claudinas 1, 3, 4, 7 e E-caderina em uma série de tumores de mama triplo-negativos.” 2012. Web. 19 Jan 2021.
Vancouver:
Cadore E. A expressão das claudinas 1, 3, 4, 7 e E-caderina em uma série de tumores de mama triplo-negativos. [Internet] [Thesis]. Universidade do Rio Grande do Sul; 2012. [cited 2021 Jan 19].
Available from: http://hdl.handle.net/10183/39662.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Cadore E. A expressão das claudinas 1, 3, 4, 7 e E-caderina em uma série de tumores de mama triplo-negativos. [Thesis]. Universidade do Rio Grande do Sul; 2012. Available from: http://hdl.handle.net/10183/39662
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
30.
栗岡, 香美.
Differential expression of the epithelial mesenchymal transition factors Snail, Slug, Twist, TGF-β, and E-cadherin in ameloblastoma : エナメル上皮腫における上皮間葉転写因子 Snail, Slug, Twist, TGF-β, E-cadherin の発現.
Degree: 博士（歯学）, 2017, Osaka Dental University / 大阪歯科大学
URL: http://id.nii.ac.jp/1392/00000142/
► Epithelial mesenchymal transition (EMT), the transition of epithelial cells into motile mesenchymal cells,plays an important role in embryogenesis, cancer invasion,and metastasis. Ameloblastomas are common epithelialodontogenic…
(more)
▼ Epithelial mesenchymal transition (EMT), the transition of epithelial cells into motile mesenchymal cells,plays an important role in embryogenesis, cancer invasion,and metastasis. Ameloblastomas are common epithelialodontogenic tumors, occurring exclusively in the mandible with locally invasive growth. Thirty-seven ameloblastoma cases were evaluated for the involvement of EMT by immunohistochemical staining and western blotting using antibodies against Slug, Snail, Twist, TGF-b, and E-cadherin. Double immunostaining was also performed. Slug and TGF-b were expressed in the nuclei of peripheral and stellate reticulum cells of ameloblastoma nests. Twenty cases of Snail, 36 of Slug, 8 of Twist, and 19 of TGF-b showed strong expression in tumor cells in follicular and plexiform patterns. Expression of Slug and TGF-b increased in regions where the expression of E-cadherin was reduced. EMT was found to be associated with thelocal invasive growth of ameloblastoma. These data suggest that reduced expression of E-cadherin and over-expression of Slug, Snail, and TGF-b induce EMT. Given that ameloblastomas are characterized by local invasiveness, EMT might be related to their development. Thus, strong expression of Slug and TGF-b and reduced expression of E-cadherin might be related to the local invasiveness of ameloblastoma.
2016年度
Subjects/Keywords: Epithelial mesenchymal transition (EMT); Ameloblastoma; Immunohistochemistry; Double immunostaining; Snail; Slug; E-cadherin
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APA ·
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APA (6th Edition):
栗岡, . (2017). Differential expression of the epithelial mesenchymal transition factors Snail, Slug, Twist, TGF-β, and E-cadherin in ameloblastoma : エナメル上皮腫における上皮間葉転写因子 Snail, Slug, Twist, TGF-β, E-cadherin の発現. (Thesis). Osaka Dental University / 大阪歯科大学. Retrieved from http://id.nii.ac.jp/1392/00000142/
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
栗岡, 香美. “Differential expression of the epithelial mesenchymal transition factors Snail, Slug, Twist, TGF-β, and E-cadherin in ameloblastoma : エナメル上皮腫における上皮間葉転写因子 Snail, Slug, Twist, TGF-β, E-cadherin の発現.” 2017. Thesis, Osaka Dental University / 大阪歯科大学. Accessed January 19, 2021.
http://id.nii.ac.jp/1392/00000142/.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
栗岡, 香美. “Differential expression of the epithelial mesenchymal transition factors Snail, Slug, Twist, TGF-β, and E-cadherin in ameloblastoma : エナメル上皮腫における上皮間葉転写因子 Snail, Slug, Twist, TGF-β, E-cadherin の発現.” 2017. Web. 19 Jan 2021.
Vancouver:
栗岡 . Differential expression of the epithelial mesenchymal transition factors Snail, Slug, Twist, TGF-β, and E-cadherin in ameloblastoma : エナメル上皮腫における上皮間葉転写因子 Snail, Slug, Twist, TGF-β, E-cadherin の発現. [Internet] [Thesis]. Osaka Dental University / 大阪歯科大学; 2017. [cited 2021 Jan 19].
Available from: http://id.nii.ac.jp/1392/00000142/.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
栗岡 . Differential expression of the epithelial mesenchymal transition factors Snail, Slug, Twist, TGF-β, and E-cadherin in ameloblastoma : エナメル上皮腫における上皮間葉転写因子 Snail, Slug, Twist, TGF-β, E-cadherin の発現. [Thesis]. Osaka Dental University / 大阪歯科大学; 2017. Available from: http://id.nii.ac.jp/1392/00000142/
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
◁ [1] [2] [3] [4] [5] [6] ▶
. 
Open Access Theses and Dissertations
