subject:(epithelial to mesenchymal transition)

University of Melbourne

1. Gunasinghe, N. P. A. Devika. Epithelial to mesenchymal transition in human breast cancer cells.

Degree: 2011, University of Melbourne

► Breast cancer is the most frequently diagnosed malignancy in females and accounts for the highest cancer related mortality worldwide. According to the available statistics, more… (more)

▼ Breast cancer is the most frequently diagnosed malignancy in females and accounts for the highest cancer related mortality worldwide. According to the available statistics, more than 90% of breast cancer related deaths occur not because of the primary tumour but as a result of the secondary metastases. Therefore, understanding the precise mechanisms involved in the progression of secondary metastases from the primary tumour is of utmost importance as a prognostic indicator for estimating metastatic risk, deciding the treatment plan, and monitoring of treatment response. The process of Epithelial to Mesenchymal Transition (EMT) has been widely accepted as a major mechanism that is involved in the metastatic cascade. The aim of the current thesis was to explore the effects of epithelial versus mesenchymal manipulation of breast cancer cells on the sequential events of metastatic progression. Since it is widely accepted that one of the cardinal features during EMT is loss or down-regulation E-cadherin, we modulated this molecule in our experimental model, the MDA-MB-468 (MDA-468) breast cancer cell line, to generate cells with a stable forced epithelial phenotype and epithelial cells with stable mesenchymal traits. The E-cadherin overexpressing cells were generated by transfecting MDA-468 cells with a plasmid vector encoding full length E-cadherin (468-CDH1), while dominant negative E-cadherin expressing cells were produced by transfecting the cells with a plasmid vector encoding a chimera of the E-cadherin cytoplasmic tail connected to the interleukin 2 receptor extracellular domain (468-dnCDH1). In addition, E-cadherin knocked down cells were generated using short hairpin technology (468-shCDH1-B and 468-shCDH1-D). The EMT-inducing effects of epidermal growth factor (EGF) and hypoxia were characterised in terms of EMT marker expression, morphology, proliferation, and migration. These assessments were also performed on the E-cadherin manipulated cells and also to examine the effects of these manipulations on EGF response. The effective introduction of each manipulation was confirmed, however, very little effect on EMT marker expression was seen. Morphology was affected by the shCDH1-mediated knock down, but not other treatments. Cell migration was inhibited by CDH1 transfection and stimulated in the most complete shCDH1 knock down, as was invasive colony outgrowth. Opposite trends on proliferation were noted, with tendencies for higher proliferation with more functional E-cadherin, and reduced proliferation in shCDH1 cells. Importantly, the published effects of EGF on apoptosis of MDA-468 cells were not seen, and instead an intense but reversible EMT was seen in the cells that became detached. Despite the lack of constitutive effects on EMT marker status, sufficient behavioural responses were seen to warrant in vivo analysis. When these E-cadherin manipulated cells were inoculated…

Subjects/Keywords: epithelial to mesenchymal transition (EMT); mesenchymal to epithelial transition (MET); breast cancer; metastasis; e-cadherin

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Gunasinghe, N. P. A. D. (2011). Epithelial to mesenchymal transition in human breast cancer cells. (Doctoral Dissertation). University of Melbourne. Retrieved from http://hdl.handle.net/11343/37325

Chicago Manual of Style (16^th Edition):

Gunasinghe, N P A Devika. “Epithelial to mesenchymal transition in human breast cancer cells.” 2011. Doctoral Dissertation, University of Melbourne. Accessed April 10, 2021. http://hdl.handle.net/11343/37325.

MLA Handbook (7^th Edition):

Gunasinghe, N P A Devika. “Epithelial to mesenchymal transition in human breast cancer cells.” 2011. Web. 10 Apr 2021.

Vancouver:

Gunasinghe NPAD. Epithelial to mesenchymal transition in human breast cancer cells. [Internet] [Doctoral dissertation]. University of Melbourne; 2011. [cited 2021 Apr 10]. Available from: http://hdl.handle.net/11343/37325.

Council of Science Editors:

Gunasinghe NPAD. Epithelial to mesenchymal transition in human breast cancer cells. [Doctoral Dissertation]. University of Melbourne; 2011. Available from: http://hdl.handle.net/11343/37325

Georgia Tech

2. Zhang, Mengnan. Analysis of the role of miRNAs in ovarian cancer metastasis.

Degree: PhD, Biology, 2019, Georgia Tech

URL: http://hdl.handle.net/1853/62647

► Cancer mortality is primarily due to metastasis. Metastasis is a complex multi-step process involving, on the molecular level, regulatory control of two key development pathways:… (more)

Subjects/Keywords: miRNA; Gene expression; Ovarian cancer; Epithelial-to-mesenchymal mesenchymal-to-epithelial transition

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Zhang, M. (2019). Analysis of the role of miRNAs in ovarian cancer metastasis. (Doctoral Dissertation). Georgia Tech. Retrieved from http://hdl.handle.net/1853/62647

Chicago Manual of Style (16^th Edition):

Zhang, Mengnan. “Analysis of the role of miRNAs in ovarian cancer metastasis.” 2019. Doctoral Dissertation, Georgia Tech. Accessed April 10, 2021. http://hdl.handle.net/1853/62647.

MLA Handbook (7^th Edition):

Zhang, Mengnan. “Analysis of the role of miRNAs in ovarian cancer metastasis.” 2019. Web. 10 Apr 2021.

Vancouver:

Zhang M. Analysis of the role of miRNAs in ovarian cancer metastasis. [Internet] [Doctoral dissertation]. Georgia Tech; 2019. [cited 2021 Apr 10]. Available from: http://hdl.handle.net/1853/62647.

Council of Science Editors:

Zhang M. Analysis of the role of miRNAs in ovarian cancer metastasis. [Doctoral Dissertation]. Georgia Tech; 2019. Available from: http://hdl.handle.net/1853/62647

Universiteit Utrecht

3. 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

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th 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 (16^th 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 April 10, 2021. http://dspace.library.uu.nl:8080/handle/1874/287101.

MLA Handbook (7^th Edition):

Pilzecker, B. “The E- and N-cadherin switch in Epithelial to Mesenchymal Transition and metastasis. Potential drug targets?.” 2013. Web. 10 Apr 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 Apr 10]. 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

4. Sultana, Shamima. Overexpression of microRNA-542-3p attenuates the differentiating capacity of endometriotic stromal cells. : miR-542-3p の過剰発現は子宮内膜症間質細胞の脱落膜化能力を低下させる.

Degree: 博士（医学）, 2018, Saitama Medical University / 埼玉医科大学

URL: http://id.nii.ac.jp/1386/00000611/

►

Endometriosis is defined as the presence of endometrial glandular and stromal cells outside of the uterine cavity. A previous study reported that microRNA (miR)-542-3p plays… (more)

Subjects/Keywords: decidualization; endometriosis; mesenchymal‐to‐epithelial transition; microRNA; migration

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Sultana, S. (2018). Overexpression of microRNA-542-3p attenuates the differentiating capacity of endometriotic stromal cells. : miR-542-3p の過剰発現は子宮内膜症間質細胞の脱落膜化能力を低下させる. (Thesis). Saitama Medical University / 埼玉医科大学. Retrieved from http://id.nii.ac.jp/1386/00000611/

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Sultana, Shamima. “Overexpression of microRNA-542-3p attenuates the differentiating capacity of endometriotic stromal cells. : miR-542-3p の過剰発現は子宮内膜症間質細胞の脱落膜化能力を低下させる.” 2018. Thesis, Saitama Medical University / 埼玉医科大学. Accessed April 10, 2021. http://id.nii.ac.jp/1386/00000611/.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Sultana, Shamima. “Overexpression of microRNA-542-3p attenuates the differentiating capacity of endometriotic stromal cells. : miR-542-3p の過剰発現は子宮内膜症間質細胞の脱落膜化能力を低下させる.” 2018. Web. 10 Apr 2021.

Vancouver:

Sultana S. Overexpression of microRNA-542-3p attenuates the differentiating capacity of endometriotic stromal cells. : miR-542-3p の過剰発現は子宮内膜症間質細胞の脱落膜化能力を低下させる. [Internet] [Thesis]. Saitama Medical University / 埼玉医科大学; 2018. [cited 2021 Apr 10]. Available from: http://id.nii.ac.jp/1386/00000611/.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Sultana S. Overexpression of microRNA-542-3p attenuates the differentiating capacity of endometriotic stromal cells. : miR-542-3p の過剰発現は子宮内膜症間質細胞の脱落膜化能力を低下させる. [Thesis]. Saitama Medical University / 埼玉医科大学; 2018. Available from: http://id.nii.ac.jp/1386/00000611/

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

NSYSU

5. Kao, Yu-Chen. Study the effects of Dibromotyrosine Derivative in TGF-Î² responsiveness.

Degree: Master, Biological Sciences, 2017, NSYSU

URL: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0718117-194840

► The Transforming growth factor Î²1 (TGF-Î²1) is belong to transforming growth factor superfamily. Many tumor lesions process are related to TGF-Î²1, such as: cell proliferation,… (more)

▼ The Transforming growth factor Î²1 (TGF-Î²1) is belong to transforming growth factor superfamily. Many tumor lesions process are related to TGF-Î²1, such as: cell proliferation, extracellular matrix secretion, cell attachment, movement, differentiation and apoptosis. TGF-Î²1 cell signaling via two protein receptors on membrane which are Type I TGF-Î² receptor (TÎ²R-I) and Type II TGF-Î² receptor (TÎ²R-II). TGF-Î² is activated that lead smad2/3 to phosphorylation, and p-Smad2/3 will transfer to nuclear than regulates the transcription of the target gene with other transcription factor. At cancer early stage, TGF-Î² will use inhibit cell proliferation and promote cell apoptosis to inhibit cancer growth, but at cancer late stage,instead, TGF-Î² will promote cancer cell growth, invasion, transfer and help it to escape the immune system attack. There are some small molecule inhibitors which can inhibit TGF-Î² cell signal transduction have great value at cancer research. Small molecule inhibitor is a powerful tool in research of signal transduction pathway interaction. In this study, we found (1â²R,5â²S,6â²S)-2-(3â²,5â²- dibromo-1â²,6â²-dihydroxy-4â²-oxocyclohex-2â²-enyl) acetonitrile (DT), a bromotyrosine derivate from Pseudoceratina sp., which inhibits the TÎ²R-I serine/threonine kinase then inhibits TGF-Î² downstream cell signaling. We use such as: luciferase activity assay, western blotting, wound healing assay, in vitro ALK5 kinase assay etc. to know the effect of DT on TGF-Î² cell signaling, and use epithelial cells to study of the inhibitory effects of DT on TGF-Î²-induced Smad signaling and epithelial-to-mesenchymal transition. We also confirmed the new ALK5 inhibitor can effectively inhibit TGF-Î² stimulate smad2/3 to phosphorylation and inhibit smad2/3 transfer to nuclear. In addition, DT also can inhibit TGF-Î² stimulate epithelial-to-mesenchymal transition and A549 cell metastasis. Our study showed DT can apply to treatment of fibrotic diseases and cancer in the future. Advisors/Committee Members: Wu, Chang-Yi (chair), Chien-Chih Chiu (chair), Wen Zhi-Hong (chair), (Chen, Chun-Lin (committee member).

Subjects/Keywords: TGF-Î²; bromotyrosine derivative; small molecular inhibitors; epithelial-to-mesenchymal transition

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Kao, Y. (2017). Study the effects of Dibromotyrosine Derivative in TGF-Î² responsiveness. (Thesis). NSYSU. Retrieved from http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0718117-194840

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Kao, Yu-Chen. “Study the effects of Dibromotyrosine Derivative in TGF-Î² responsiveness.” 2017. Thesis, NSYSU. Accessed April 10, 2021. http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0718117-194840.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Kao, Yu-Chen. “Study the effects of Dibromotyrosine Derivative in TGF-Î² responsiveness.” 2017. Web. 10 Apr 2021.

Vancouver:

Kao Y. Study the effects of Dibromotyrosine Derivative in TGF-Î² responsiveness. [Internet] [Thesis]. NSYSU; 2017. [cited 2021 Apr 10]. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0718117-194840.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Kao Y. Study the effects of Dibromotyrosine Derivative in TGF-Î² responsiveness. [Thesis]. NSYSU; 2017. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0718117-194840

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Penn State University

6. Dang, Hien T. The Regulatioon of Mesenchymal and cancer stem cell phenotypes in hepatocellular carcinoma.

Degree: 2012, Penn State University

URL: https://submit-etda.libraries.psu.edu/catalog/15868

► Hepatocellular carcinoma (HCC) is one of the most common malignancies worldwide and is the third leading cause of cancer deaths. Unfortunately, patients with HCC present… (more)

▼ Hepatocellular carcinoma (HCC) is one of the most common malignancies worldwide and is the third leading cause of cancer deaths. Unfortunately, patients with HCC present with invasive/metastatic disease that is resistant to traditional cytotoxic treatment and are not eligible for curative therapy such as surgical resection or liver transplantation. Increasing evidence indicates that cancer stem cells (CSCs) are the origin of a subset of HCC. Furthermore, the epithelial-to-mesenchymal transition (EMT) program has been demonstrated to generate cells with CSC characteristics. Resistance to therapy and metastatic disease are two factors that correlate a progenitor-phenotype in HCC with poor survival. The EMT program allows epithelial cells to migrate and intravasate into the blood stream and metastasize to distant organ sites. Accordingly, these disseminated cancer cells require self-renewal capability and other characteristics similar to those exhibited by stem cells in order to survive and promote tumor initiation. These observations lead to the hypothesis that the EMT program is responsible for generating stem-like cells that can spawn macroscopic metastases. Our central hypothesis is that cancer stem cells and the EMT program are linked through central regulators such as the TGF and c-Met/HGF signaling axes, and that targeting these mechanisms will improve the design of novel therapeutics for advanced HCC. In murine epithelial HCC cells, TGFinduced EMT through Snail1 is indicated by CSC characteristics including increased tumorsphere formation (self-renewal assay) and increased CSC-related genes including CD44, Nanog, and Bmi-1. We demonstrated that Snail1 induced a CSC phenotype through the regulation of the Nanog promoter and that the inhibition of Snail1 leads to the loss of the EMT and CSC phenotypes. In both CSC and EMT-like murine and human HCC cells, CD44 mRNA expression was high; thus we hypothesized that CD44 plays a central role in regulating the CSC and EMT phenotypes. CD44 undergoes alternative splicing, generating multiple splice variants, each with a different function. Recent evidence indicates that CD44s (CD44 standard form) regulates EMT. c-Met has been demonstrated to regulate CD44 splicing and c-Met+ HCC cells demonstrated a mesenchymal phenotype with CSC characteristics including increased CD44s expression and tumorsphere formation capability. To investigate the regulation of CD44s by c-Met, we inhibited c-Met signaling. The down regulation of c-Met decreased CD44s expression and decreased CSC and EMT phenotypes. Further analysis demonstrated that c-Met regulates CD44s through p-AKT and that subsequent loss of CD44s leads to decreased EMT and CSC characteristics in the human MHCC97-H cell line. To further document that c-Met regulates tumor initiation through CD44s, we knocked down CD44s in MHCC97-H cells. The down regulation of CD44s produced loss of both the EMT and CSC phenotype, minimal change in c-Met signaling. In vivo data demonstrates that CD44s is required for tumor initiation.… Advisors/Committee Members: Kent Eugene Vrana, Dissertation Advisor/Co-Advisor, Kent Eugene Vrana, Committee Chair/Co-Chair, Bill Freeman, Committee Member, Charles H Lang, Committee Member, Harriet C Isom, Committee Member.

Subjects/Keywords: liver cancer; cancer stem cells; epithelial to mesenchymal transition

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Dang, H. T. (2012). The Regulatioon of Mesenchymal and cancer stem cell phenotypes in hepatocellular carcinoma. (Thesis). Penn State University. Retrieved from https://submit-etda.libraries.psu.edu/catalog/15868

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Dang, Hien T. “The Regulatioon of Mesenchymal and cancer stem cell phenotypes in hepatocellular carcinoma.” 2012. Thesis, Penn State University. Accessed April 10, 2021. https://submit-etda.libraries.psu.edu/catalog/15868.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Dang, Hien T. “The Regulatioon of Mesenchymal and cancer stem cell phenotypes in hepatocellular carcinoma.” 2012. Web. 10 Apr 2021.

Vancouver:

Dang HT. The Regulatioon of Mesenchymal and cancer stem cell phenotypes in hepatocellular carcinoma. [Internet] [Thesis]. Penn State University; 2012. [cited 2021 Apr 10]. Available from: https://submit-etda.libraries.psu.edu/catalog/15868.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Dang HT. The Regulatioon of Mesenchymal and cancer stem cell phenotypes in hepatocellular carcinoma. [Thesis]. Penn State University; 2012. Available from: https://submit-etda.libraries.psu.edu/catalog/15868

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Toronto

7. Brethour, Dylan Edward. PrP and its Ancestral Relatives ZIP6 and ZIP10 Interact with NCAM1, Altering its Molecular Environment and Post-translational Modifications during Epithelial-to-mesenchymal Transition.

Degree: 2016, University of Toronto

URL: http://hdl.handle.net/1807/80225

►

The prion protein (PrP) was recently found to be evolutionarily linked to a subfamily of ZIP transporters which possess a PrP-like domain. A member of… (more)

Subjects/Keywords: epithelial-to-mesenchymal transition; mass spectrometry; ncam; prion protein; ZIP6; 0317

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Brethour, D. E. (2016). PrP and its Ancestral Relatives ZIP6 and ZIP10 Interact with NCAM1, Altering its Molecular Environment and Post-translational Modifications during Epithelial-to-mesenchymal Transition. (Masters Thesis). University of Toronto. Retrieved from http://hdl.handle.net/1807/80225

Chicago Manual of Style (16^th Edition):

Brethour, Dylan Edward. “PrP and its Ancestral Relatives ZIP6 and ZIP10 Interact with NCAM1, Altering its Molecular Environment and Post-translational Modifications during Epithelial-to-mesenchymal Transition.” 2016. Masters Thesis, University of Toronto. Accessed April 10, 2021. http://hdl.handle.net/1807/80225.

MLA Handbook (7^th Edition):

Brethour, Dylan Edward. “PrP and its Ancestral Relatives ZIP6 and ZIP10 Interact with NCAM1, Altering its Molecular Environment and Post-translational Modifications during Epithelial-to-mesenchymal Transition.” 2016. Web. 10 Apr 2021.

Vancouver:

Brethour DE. PrP and its Ancestral Relatives ZIP6 and ZIP10 Interact with NCAM1, Altering its Molecular Environment and Post-translational Modifications during Epithelial-to-mesenchymal Transition. [Internet] [Masters thesis]. University of Toronto; 2016. [cited 2021 Apr 10]. Available from: http://hdl.handle.net/1807/80225.

Council of Science Editors:

Brethour DE. PrP and its Ancestral Relatives ZIP6 and ZIP10 Interact with NCAM1, Altering its Molecular Environment and Post-translational Modifications during Epithelial-to-mesenchymal Transition. [Masters Thesis]. University of Toronto; 2016. Available from: http://hdl.handle.net/1807/80225

University of Iowa

8. Nauseef, Jones Trevor. An investigation of the molecular and biophysical properties of metastatic cells.

Degree: PhD, Molecular Physiology and Biophysics, 2015, University of Iowa

URL: https://ir.uiowa.edu/etd/3150

► Prostate cancer presents a significant paradox: it is very common, yet rarely fatal. To wit, the prostate is the most common non-skin tissue for… (more)

▼ Prostate cancer presents a significant paradox: it is very common, yet rarely fatal. To wit, the prostate is the most common non-skin tissue for cancer diagnosis in men in the United States. Despite its high incidence, fatal malignancy occurs in only a small fraction of diagnosed men. The fatal cases are characteristically defined by distant spread in the body, also known as metastasis. In order to metastasize a cancer cell must complete several sequential steps. These include degradation of and invasion through the epithelial basement membrane, typically through the loss of static intracellular adhesions with fellow epithelial cells; entrance into the blood stream (intravasation); survival within circulation; exit from the blood stream upon arrival at a new tissue (extravasation); and survival and colonization at the secondary site. At the time of diagnosis, it is not currently possible to accurately predict future metastasis and thereby clinicians cannot delineate those men at high risk for fatal disease from the vast majority of men who are likely to experience an indolent disease course. Consequently, we examined the behavior of cancer cells in several steps of the metastatic cascade. In doing so, we uncovered both molecular and biophysical characteristics of cancer cells that may facilitate successful metastatic dissemination and tumor outgrowth. Epithelial-to-mesenchymal transition (EMT) is physiological process of transdifferentiation that is normally initiated during vertebrate development, but has recently been implicated in tumor development, progression, and metastases. The EMT program results in dramatic changes, including the exchange of epithelial for mesenchymal markers, altered cellular morphology, and gain of motility. EMT-like cellular alterations have been implicated most strongly in the metastasis steps of invasion and survival of cells at primary tumors sites. How EMT-like changes may facilitate survival and growth in the microenvironment of a micrometastatic niche has been less clearly elucidated. Consequently, we evaluated how EMT-like changes may affect the survival and subsequent outgrowth of prostate cancer cell lines following restrictive growth conditions. We observed that EMT-like cells as compared to their more epithelial counterparts displayed enhanced maintenance of their proliferative potential following extended culture in nutrient restriction. This phenotype depended on an EMT-associated increase in autophagy. Notably, the post-stress outgrowth phenotype could be conferred through a paracrine signaling mechanism that may involve autophagy-derived exosome-like extracellular vesicles. These studies demonstrated that EMT-like cells have a resistance to nutrient restriction through enhanced autophagy and may have uncovered a novel autophagy-dependent exosomal secretion pathway. Metastatic efficiency is thought to be strongly limited by the destruction of circulating tumor cells by the hemodynamic shear forces within the vasculature. However,… Advisors/Committee Members: Henry, Michael D. (supervisor).

Subjects/Keywords: publicabstract; Biophysics; Cancer; Epithelial to mesenchymal transition; Metastasis; Microfluidics; Biophysics

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Nauseef, J. T. (2015). An investigation of the molecular and biophysical properties of metastatic cells. (Doctoral Dissertation). University of Iowa. Retrieved from https://ir.uiowa.edu/etd/3150

Chicago Manual of Style (16^th Edition):

Nauseef, Jones Trevor. “An investigation of the molecular and biophysical properties of metastatic cells.” 2015. Doctoral Dissertation, University of Iowa. Accessed April 10, 2021. https://ir.uiowa.edu/etd/3150.

MLA Handbook (7^th Edition):

Nauseef, Jones Trevor. “An investigation of the molecular and biophysical properties of metastatic cells.” 2015. Web. 10 Apr 2021.

Vancouver:

Nauseef JT. An investigation of the molecular and biophysical properties of metastatic cells. [Internet] [Doctoral dissertation]. University of Iowa; 2015. [cited 2021 Apr 10]. Available from: https://ir.uiowa.edu/etd/3150.

Council of Science Editors:

Nauseef JT. An investigation of the molecular and biophysical properties of metastatic cells. [Doctoral Dissertation]. University of Iowa; 2015. Available from: https://ir.uiowa.edu/etd/3150

University of Illinois – Chicago

9. Li, Yanyang. Proteomic Characterization of Embryonic Epicardial-Myocardial Signaling.

Degree: 2017, University of Illinois – Chicago

URL: http://hdl.handle.net/10027/21930

► The communication between the epicardium and the underlying myocardium is crucial not only for proper heart development but also for homeostasis and response to injury… (more)

▼ The communication between the epicardium and the underlying myocardium is crucial not only for proper heart development but also for homeostasis and response to injury in the adult heart. Studies of epicardial-myocardial signaling using targeted approaches have yielded many insights into the molecular basis of this communication. Still, the complex molecular interactions and regulatory networks involved in the epicardial-myocardial crosstalk are not well understood. To obtain a comprehensive, unbiased perspective on epicardial/myocardial signaling, we used a discovery-based proteomics approach that complements traditional targeted approaches. This thesis details the generation of an unbiased dataset of proteins secreted into the media by embryonic chicken epicardial-derived cells (EPDC)-heart explant (EHE) co-cultures. A 150-protein secretome dataset was then generated by integrating mass spectrometry with bioinformatics. The large size of the dataset enabled bioinformatics analysis to deduce networks for the regulation of specific biological processes and predicted signal transduction nodes within the networks. Functional analysis was performed on one of the predicted nodes, NF-κB, and demonstrated that NF-κB activation is an essential step in TGFβ2/PDGFBB-induced cardiac epithelial-to-mesenchymal transition. Taken together, we have generated an unbiased EHE secretome dataset for the first time. Bioinformatics analysis of the dataset successfully predicted an essential role for NF-κB in epicardial EMT, indicating that this dataset can be used to guide functional, and targeted investigation. Epicardial-myocardial crosstalk occurs in vivo in the sub-epicardial niche. To complement our ex vivo culture system-based proteomic study, I explored the feasibility of developing a matrix-assisted laser desorption/ionization imaging mass spectrometry (MALDI-IMS) protocol for untargeted detection and imaging of endogenous proteins/peptides on mouse heart sections. Intact protein imaging on embryonic heart sections demonstrated the feasibility of achieving images with sufficient spatial resolution targeted to the epicardium/subepicardium area. However, in situ protein identification only detected the most abundant proteins, with no additional secreted proteins identified. These results suggest further technology development is needed to identify low abundance proteins directly from tissue sections. Advisors/Committee Members: Kay, Brian (advisor), Orenic, Teresa (committee member), Simon, Hans-Georg (committee member), Wang, Q. Tian (committee member), Okkema, Peter (chair).

Subjects/Keywords: Cardiovascular development; NF-κB; Epithelial-to-Mesenchymal Transition; Mass spectrometry

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Li, Y. (2017). Proteomic Characterization of Embryonic Epicardial-Myocardial Signaling. (Thesis). University of Illinois – Chicago. Retrieved from http://hdl.handle.net/10027/21930

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Li, Yanyang. “Proteomic Characterization of Embryonic Epicardial-Myocardial Signaling.” 2017. Thesis, University of Illinois – Chicago. Accessed April 10, 2021. http://hdl.handle.net/10027/21930.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Li, Yanyang. “Proteomic Characterization of Embryonic Epicardial-Myocardial Signaling.” 2017. Web. 10 Apr 2021.

Vancouver:

Li Y. Proteomic Characterization of Embryonic Epicardial-Myocardial Signaling. [Internet] [Thesis]. University of Illinois – Chicago; 2017. [cited 2021 Apr 10]. Available from: http://hdl.handle.net/10027/21930.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Li Y. Proteomic Characterization of Embryonic Epicardial-Myocardial Signaling. [Thesis]. University of Illinois – Chicago; 2017. Available from: http://hdl.handle.net/10027/21930

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Princeton University

10. Ell, Brian James. Tumor-Intrinsic and -Extrinsic Mechanisms in Breast Cancer Metastasis .

Degree: PhD, 2013, Princeton University

URL: http://arks.princeton.edu/ark:/88435/dsp015x21tf54k

► In breast cancer, mortality is predominantly associated with metastasis, cancerous spread to distant organs. Understanding tumor dissemination is vitally important to continued therapeutic advancement, but… (more)

▼ In breast cancer, mortality is predominantly associated with metastasis, cancerous spread to distant organs. Understanding tumor dissemination is vitally important to continued therapeutic advancement, but research is hindered by the inherent complexity within the metastatic cascade, including tumor-intrinsic and tumor-extrinsic mechanisms. This dissertation examines the interplay between these processes, defining methods by which tumor cells disseminate and uncovering novel metastasis therapies. The first study examines the mechanism by which tumor cells influence osteoclast differentiation, a crucial component of osteolytic metastasis. We report broad microRNA (miRNA) expression changes in osteoclasts after exposure to tumor-conditioned media, due in part to NFκB signaling by soluble intracellular adhesion molecule (sICAM1) from bone-metastatic cells. Ectopic expression of multiple miRNAs suppressed osteoclast differentiation by targeting important osteoclast genes. In vivo delivery of these miRNAs inhibited osteoclast activity and reduced osteolytic bone metastasis. Functional studies revealed impaired osteoclast development, and reduced bone metastasis burden, after ectopic expression of miR-141 and miR-219. These findings establish miRNAs as potential therapeutic targets and clinical biomarkers of bone metastasis via a tumor-extrinsic mechanism. The second and third studies examine tumor-intrinsic mechanisms involved in breast cancer lung metastasis. The miR-23b/27b/24 miRNAs were associated with lung metastasis samples from human patients, and correlated with increased metastatic potential in breast cancer cell lines. Ectopic expression of the miRNAs in weakly metastatic cells inhibited in vitro migration, but enhanced metastasis. MiR-24 and miR-27b were found to target Prosaposin, a protein with potential metastasis-suppressing functions. The final section examines the dynamics of TGFβ-induced epithelial-to-mesenchymal transition (EMT). Utilizing a mathematical model, we examined cellular commitment to EMT during the first steps of metastasis. Our findings show that EMT is predicated by a positive feedback loop between transcription factors and regulatory miRNAs. This feedback loop produces a bistable, hysteretic system, in which picomolar concentrations of TGFβ are capable of inducing a stable EMT. Furthermore, TGFβ functions through an autocrine pathway, producing additional TGFβ that influences surrounding cells. In vivo analysis found that hysteresis within TGFβ-induced EMT is capable of enhancing metastasis. These results further the understanding of miRNAs and EMT during metastasis, and suggest additional therapeutic strategies. Advisors/Committee Members: Kang, Yibin (advisor).

Subjects/Keywords: Breast Cancer; Epithelial-to-mesenchymal transition; Metastasis; MicroRNA; Osteoclast

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Ell, B. J. (2013). Tumor-Intrinsic and -Extrinsic Mechanisms in Breast Cancer Metastasis . (Doctoral Dissertation). Princeton University. Retrieved from http://arks.princeton.edu/ark:/88435/dsp015x21tf54k

Chicago Manual of Style (16^th Edition):

Ell, Brian James. “Tumor-Intrinsic and -Extrinsic Mechanisms in Breast Cancer Metastasis .” 2013. Doctoral Dissertation, Princeton University. Accessed April 10, 2021. http://arks.princeton.edu/ark:/88435/dsp015x21tf54k.

MLA Handbook (7^th Edition):

Ell, Brian James. “Tumor-Intrinsic and -Extrinsic Mechanisms in Breast Cancer Metastasis .” 2013. Web. 10 Apr 2021.

Vancouver:

Ell BJ. Tumor-Intrinsic and -Extrinsic Mechanisms in Breast Cancer Metastasis . [Internet] [Doctoral dissertation]. Princeton University; 2013. [cited 2021 Apr 10]. Available from: http://arks.princeton.edu/ark:/88435/dsp015x21tf54k.

Council of Science Editors:

Ell BJ. Tumor-Intrinsic and -Extrinsic Mechanisms in Breast Cancer Metastasis . [Doctoral Dissertation]. Princeton University; 2013. Available from: http://arks.princeton.edu/ark:/88435/dsp015x21tf54k

University of Minnesota

11. Fairchild, Corinne Leigh Alinea. Restricting cell movement: the role of Tspan18 in neural crest migration.

Degree: PhD, 2013, University of Minnesota

URL: http://purl.umn.edu/157977

► The neural crest is a unique population of stem cells that arise from the developing central nervous system of vertebrate embryos. Unlike surrounding neuroepithelial cells,… (more)

▼ The neural crest is a unique population of stem cells that arise from the developing central nervous system of vertebrate embryos. Unlike surrounding neuroepithelial cells, neural crest cells undergo an epithelial-to-mesenchymal transition (EMT) and migrate into the periphery of the embryo where they contribute to diverse adult lineages, including the central nervous system, craniofacial skeleton and melanocytes. Despite the fundamental importance of the neural crest, our understanding of the molecular events controlling neural crest migration is incomplete. My thesis focuses on how the transmembrane scaffolding protein, Tetraspanin18 (Tspan18) regulates neural crest EMT. Here I show that Tspan18 is expressed in premigratory, cranial neural crest cells, but is downregulated prior to migration. Sustained expression of Tspan18 maintains the epithelial cell adhesion molecule cadherin-6B (Cad6B) post-translationally, without affecting Cad6B mRNA levels, and in turn inhibits cranial neural crest migration. In contrast, morpholino-mediated knockdown of Tspan18 reduces Cad6B protein levels. Unexpectedly, this does not lead to precocious migration, emphasizing that although loss of Tspan18 is required for migration, loss of Tspan18 alone is not sufficient to trigger neural crest migration. This is, at least in part, because EMT is a multiple step process, and the other steps of EMT are not affected by Tspan18 knockdown. Together these findings suggest that Tspan18 antagonizes neural crest EMT by supporting cell adhesion. Additionally, I show here that Tspan18 downregulation at the onset of migration is achieved by the winged-helix transcription factor, FoxD3. FoxD3 knockdown sustains Tspan18 mRNA levels and inhibits neural crest formation and migration. Importantly, Tspan18 knockdown rescues the FoxD3 loss-of-function migration defect without rescuing the reduction in neural crest cell number. This suggests that FoxD3 independently regulates neural crest formation and migration, and effects migration through its regulation of Tspan18. Overall, the work in this thesis has defined a novel, Tspan18-dependent maintenance of Cad6B protein levels in epithelial cranial neural crest cells that is relieved, via FoxD3, to support migration. This work provides important insight into how cell adhesion molecules are regulated during EMT and increases our understanding for how neural crest transcription factors, like FoxD3, impact the cellular events that lead to migration.

Subjects/Keywords: Cadherin; Epithelial-to-mesenchymal transition (EMT); FoxD3; Neural crest; Tetraspanin

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Fairchild, C. L. A. (2013). Restricting cell movement: the role of Tspan18 in neural crest migration. (Doctoral Dissertation). University of Minnesota. Retrieved from http://purl.umn.edu/157977

Chicago Manual of Style (16^th Edition):

Fairchild, Corinne Leigh Alinea. “Restricting cell movement: the role of Tspan18 in neural crest migration.” 2013. Doctoral Dissertation, University of Minnesota. Accessed April 10, 2021. http://purl.umn.edu/157977.

MLA Handbook (7^th Edition):

Fairchild, Corinne Leigh Alinea. “Restricting cell movement: the role of Tspan18 in neural crest migration.” 2013. Web. 10 Apr 2021.

Vancouver:

Fairchild CLA. Restricting cell movement: the role of Tspan18 in neural crest migration. [Internet] [Doctoral dissertation]. University of Minnesota; 2013. [cited 2021 Apr 10]. Available from: http://purl.umn.edu/157977.

Council of Science Editors:

Fairchild CLA. Restricting cell movement: the role of Tspan18 in neural crest migration. [Doctoral Dissertation]. University of Minnesota; 2013. Available from: http://purl.umn.edu/157977

University of Melbourne

12. Nguyen, Linh My. Effects of chemotherapy on colorectal liver metastases.

Degree: 2012, University of Melbourne

URL: http://hdl.handle.net/11343/37303

► Background: Colorectal cancer (CRC) is the fourth most frequently occurring cancer in the world. Despite optimum surgical endeavours, many patients will develop disease recurrence. Treatments… (more)

▼ Background: Colorectal cancer (CRC) is the fourth most frequently occurring cancer in the world. Despite optimum surgical endeavours, many patients will develop disease recurrence. Treatments available for patients who do not qualify for surgical resection are limited and mainly consist of chemotherapy or radiotherapy. Recent innovative options focus on selective targeting of the tumour blood supply, as a means of achieving greater tumour destruction or slowing overall tumour progression. Two main classes of drugs have been used both clinically and experimentally: the angioinhibitory agents (AIA) that inhibit the formation of new vessels, and the vascular disruptive agents (VDA) that target endothelial cells in immature tumour vessels, causing vessel collapse, tumour hypoxia and death. Treatment by VDAs are characterised by rapid and extensive destruction of tumour limited only by the persistence of a viable rim of tumour cells in the periphery, which subsequently leads to recurrence. The VDA OXi4503 is one of the most potent VDAs being tested, and our own research has demonstrated a rapid onset of microvascular thrombosis leading to tumour necrosis in excess of 90% of the tumour. Despite this efficacy, complete tumour eradication was not achieved as a thin rim of viable tumour invariably survived in the periphery giving rise to recurrence. Understanding the mechanisms that enable tumour to survive in the periphery could lead to formulation of drug combinations for total tumour eradication. Based on the finding that only tumour cells in the periphery survive the VDA treatment this study tests the following hypotheses: • Morphological and molecular differences in the tumour contribute to drug resistance in the tumour periphery (Chapter 4). • Treatment with OXi4503 promotes molecular and morphological changes in the residual tumour rendering the tumour resistant to cytotoxic treatments (Chapter 5 and Chapter 6). • Combination treatment using AIA (Sunitinib) and VDA (OXi4503) may produce complete destruction of colorectal liver tumours and hence improve treatment outcomes (Chapter 7). Experimental Design: Using a murine colorectal liver metastases model, inherent morphological and molecular differences within the periphery and the centre of the tumour that may account for differences in resistance to OXi4503 treatment were investigated. H&E staining and immunostaining were used to examine spatial differences in vessel maturity and stability, accumulation of immune cells, the expression of proangiogenic factors/receptors (HIF-1α, VEGF and ATR1) and the expression of epithelial to mesenchymal transition (EMT) markers (ZEB1, vimentin, E-cadherin and β-catenin) between the periphery and the centre of established tumours. The effects of single dose OXi4503 treatment on tumour vessels, cell kinetics, changes in growth factors (HIF-1α, VEGF and…

Subjects/Keywords: OXi4503; Sunitinib; epithelial to mesenchymal transition; colorectal liver metastases

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Nguyen, L. M. (2012). Effects of chemotherapy on colorectal liver metastases. (Doctoral Dissertation). University of Melbourne. Retrieved from http://hdl.handle.net/11343/37303

Chicago Manual of Style (16^th Edition):

Nguyen, Linh My. “Effects of chemotherapy on colorectal liver metastases.” 2012. Doctoral Dissertation, University of Melbourne. Accessed April 10, 2021. http://hdl.handle.net/11343/37303.

MLA Handbook (7^th Edition):

Nguyen, Linh My. “Effects of chemotherapy on colorectal liver metastases.” 2012. Web. 10 Apr 2021.

Vancouver:

Nguyen LM. Effects of chemotherapy on colorectal liver metastases. [Internet] [Doctoral dissertation]. University of Melbourne; 2012. [cited 2021 Apr 10]. Available from: http://hdl.handle.net/11343/37303.

Council of Science Editors:

Nguyen LM. Effects of chemotherapy on colorectal liver metastases. [Doctoral Dissertation]. University of Melbourne; 2012. Available from: http://hdl.handle.net/11343/37303

University of Melbourne

13. Chen, Anna. Investigating the role of hypoxia in tumour progression in breast cancer.

Degree: 2015, University of Melbourne

URL: http://hdl.handle.net/11343/92001

► Metastasis is a major cause of morbidity and mortality in breast cancer patients. The molecular processes and mediators that underpin this process have yet to… (more)

▼ Metastasis is a major cause of morbidity and mortality in breast cancer patients. The molecular processes and mediators that underpin this process have yet to be completely delineated. Hypoxia, the state of reduced oxygen conditions, occurs frequently in solid tumours and is a factor of poor prognosis for patient outcome. The upregulation of HIF-1α, the main mediator of the hypoxic response pathway, has been implicated in several different facets of tumour progression, including tumour growth, angiogenesis, therapy resistance and metastasis. Hypoxia has been shown to induce Epithelial-to-Mesenchymal Transition (EMT), a highly conserved developmental program that facilitates tumour cell dissemination. It is thought that EMT is co-opted by epithelial tumour cells in order to acquire a degree of plasticity, allowing them to undergo a number of genetic, biochemical and morphological changes to adopt a mesenchymal phenotype. This results in the loss of polarity, and the gain of migratory and invasive capabilities. EMT is regulated by a core cassette of transcription factors, including Snail, Slug, Twist, Zeb1 and Zeb2. Zeb1 is the most proximal transcription factor, however, how hypoxia modulates Zeb1 expression is not known. This study demonstrates that Siah, a family of E3 ubiquitin ligases and a master regulator of HIF-1α protein expression, binds to and targets Zeb1 for proteasomal degradation. Loss of Siah2 is sufficient to cause spontaneous EMT in tumour cells derived from the PyMT murine model of breast cancer. On the other hand, EMT induction led to the decrease in Siah protein expression. This work is the first to describe a post-translational mechanism of regulation of Zeb1 and further defines the relationship between hypoxia and EMT. There are, in fact, two forms of hypoxia in a growing tumour, chronic hypoxia and intermittent hypoxia. Chronic hypoxia describes the long-term limitations on oxygen diffusion caused by abnormal tumour vasculature. While intermittent hypoxia refers to the fluctuations of oxygen tension in a tumour, caused by the aberrant and temporary closing and reopening of tumour-supplying blood vessels. The consequences of these two different types of hypoxia in breast cancer have not yet been well characterised. Using the orthotopic, syngeneic PyMT murine model of breast cancer, it was found that intermittent hypoxia-treated cells gave rise to a greater number of larger lung metastases in vivo. This was facilitated by an enhanced ability for anchorage-independent growth, increased clonogenicity, the induction of a pro-tumourigenic gene expression and secretory profile, and the increase in tumour-initiating capacity through the gain of cancer stem cell properties. RNA sequencing of hypoxia-treated cells found distinct gene expression patterns between treatment groups. While, pathway analysis revealed a marked enrichment of immune-related pathways and a downregulation of DNA replication and cell cycle pathways, by both chronic and intermittent hypoxia. Interestingly, chronic hypoxia…

Subjects/Keywords: breast cancer; hypoxia; metastasis; epithelial-to-mesenchymal transition; tumour microenvironment

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Chen, A. (2015). Investigating the role of hypoxia in tumour progression in breast cancer. (Doctoral Dissertation). University of Melbourne. Retrieved from http://hdl.handle.net/11343/92001

Chicago Manual of Style (16^th Edition):

Chen, Anna. “Investigating the role of hypoxia in tumour progression in breast cancer.” 2015. Doctoral Dissertation, University of Melbourne. Accessed April 10, 2021. http://hdl.handle.net/11343/92001.

MLA Handbook (7^th Edition):

Chen, Anna. “Investigating the role of hypoxia in tumour progression in breast cancer.” 2015. Web. 10 Apr 2021.

Vancouver:

Chen A. Investigating the role of hypoxia in tumour progression in breast cancer. [Internet] [Doctoral dissertation]. University of Melbourne; 2015. [cited 2021 Apr 10]. Available from: http://hdl.handle.net/11343/92001.

Council of Science Editors:

Chen A. Investigating the role of hypoxia in tumour progression in breast cancer. [Doctoral Dissertation]. University of Melbourne; 2015. Available from: http://hdl.handle.net/11343/92001

University of South Florida

14. Richards, Edward J. Function of Long Noncoding RNAs in Breast Cancer.

Degree: 2015, University of South Florida

URL: https://scholarcommons.usf.edu/etd/5767

► Breast cancer is a disease that will be diagnosed in about 1 in 10 women throughout their lifetime. The majority of breast cancers are originated… (more)

▼ Breast cancer is a disease that will be diagnosed in about 1 in 10 women throughout their lifetime. The majority of breast cancers are originated from the epithelial cells of the mammary ducts, and this occurrence can be due to several factors including hereditary and acquired mutation. There are several major breast cancer subtypes, including estrogen receptor-α (ERα)-positive, HER2-enriched and triple-negative (TNBC). Patients diagnosed with ER+ tumors are generally treated with estrogen blockers (e.g., tamoxifen, letrozole and fulvestrant). Patients with HER2+ tumors are commonly administered with drugs that block HER2 signaling (e.g., trastuzumab) or inhibit HER2’s tyrosine kinase activity (e.g., lapatinib). For patients with TNBC, chemotherapies such as taxanes and anthracyclines are standard of care therapies. However, for each breast cancer subtype, a significant number of patients develop resistance to these therapies and eventually die from metastasis, a process which accounts for ~90% of breast cancer mortality. Currently, metastatic breast cancer is incurable, and the short median survival of 3 years for patients with metastatic breast cancer has not significantly changed in over 20 years. Therefore identification of new molecules that are involved in breast cancer metastasis and development of more precisely targeted therapeutic strategies are urgently needed to improve the clinical outcome for this disease. The transforming growth factor pathway beta (TGFβ) pathway has been show to play a key role in metastasis through induction of epithelial-mesenchymal transition (EMT), cell migration and invasion. Over more than a decade, this pathway has been studied across several cancers and it is now better established that it has context-dependent tumor suppressive and oncogenic qualities. In the early stages of breast cancer, TGFβ pathway is a suppressor of benign and early stage tumor growth. However, as disease progresses and corresponding levels of TGFβ ligands become elevated, a “switch” will take place and promote oncogenic phenotypes like EMT and cancer cell stemness which drive metastasis. Long noncoding RNAs (lncRNAs) are an emerging subclass of RNA molecules in cancer biology. LncRNAs are >200nt and can influence target gene expression locally in “cis”, or along a distant chromosome in “trans”, through various mechanisms and interactions with other biological molecules. The contribution of TGFβ-regulated lncRNAs to associated phenotypes like EMT and cancer cell stemness has not been very well studied. The aim of this doctoral dissertation is to address the functional and mechanistic roles of lncRNAs in these processes. Using a well-established TGFβ-induced EMT model (e.g., mouse mammary epithelial cell NMuMG treated with TGFβ, we have identified 3 conserved lncRNAs (lncRNA-HIT, WDFY3-AS2 and TIL) that are significantly upregulated upon TGFβ-induced EMT. They all mediate TGFβ-induced EMT, cell migration and invasion. Overexpression of these lncRNAs is frequently detected during the breast cancer…

Subjects/Keywords: TGFβ; epithelial to mesenchymal transition; metastasis; Cell Biology; Molecular Biology

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Richards, E. J. (2015). Function of Long Noncoding RNAs in Breast Cancer. (Thesis). University of South Florida. Retrieved from https://scholarcommons.usf.edu/etd/5767

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Richards, Edward J. “Function of Long Noncoding RNAs in Breast Cancer.” 2015. Thesis, University of South Florida. Accessed April 10, 2021. https://scholarcommons.usf.edu/etd/5767.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Richards, Edward J. “Function of Long Noncoding RNAs in Breast Cancer.” 2015. Web. 10 Apr 2021.

Vancouver:

Richards EJ. Function of Long Noncoding RNAs in Breast Cancer. [Internet] [Thesis]. University of South Florida; 2015. [cited 2021 Apr 10]. Available from: https://scholarcommons.usf.edu/etd/5767.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Richards EJ. Function of Long Noncoding RNAs in Breast Cancer. [Thesis]. University of South Florida; 2015. Available from: https://scholarcommons.usf.edu/etd/5767

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Edinburgh

15. Petrovich, Giulia. Investigating the differential instructive roles of WT1's isoforms.

Degree: PhD, 2016, University of Edinburgh

URL: http://hdl.handle.net/1842/23423

► The Wilms' tumour suppressor gene Wt1 is a key regulator of embryonic development and tissue homeostasis. In humans, mutation in the gene may lead to… (more)

▼ The Wilms' tumour suppressor gene Wt1 is a key regulator of embryonic development and tissue homeostasis. In humans, mutation in the gene may lead to childhood kidney cancer, severe glomerular kidney diseases, gonadal dysgenesis and, in rare cases, heart diseases. The importance of WT1 in embryonic development is related to its crucial function in the regulation of two cellular plasticity processes: the epithelial to mesenchymal transition (EMT) and the reverse process, the mesenchymal to epithelial transition (MET). WT1 expression persists during the waves of EMT and MET that generate certain mesodermal tissues. In fact, WT1 is a major regulator of both transitions and it is essential for the survival of mesenchyme progenitors. Furthermore, it has been proposed that WT1 is required for the derivation of progenitors from different mesothelia, possibly through an EMT. Progenitors expressing WT1 are believed to differentiate into different cell types, giving rise to coronary vasculature, adipocytes and hepatic stellate cells. In my PhD I aimed to investigate the instructive role of different WT1 isoforms. To address this, the first goal was to generate a single plasmid that would accommodate all necessary components of an inducible system, in order to derive cellular models for the inducible expression of WT1 single isoforms. Second, I aimed to understand the processes that the single variants were sufficient to drive. Therefore, I started with the establishment of two cellular models for the inducible expression of the main four isoforms of WT1 (with or without the exon 5 and/or the KTS, here referred as +/+, +/-, -/+ and -/-). I cloned different plasmids carrying doxycycline inducible WT1 isoforms and derived single stable clones in two epithelial kidney cell lines that do not express WT1: the MDCK and the IMCD3 cells. I then analysed the expression profiles of the clones, using either microarray or RNA sequencing, and performed cellular assays to characterize the cells after WT1 induction. Overall, WT1 induction did not affect cell growth, cell cycle, cell migration or anchorage independent growth, suggesting that the expression of WT1 in these two cell lines does not change their oncogenic potential. The expression analysis of the MDCK cells suggested that the induction of WT1 isoforms activates an inflammatory response, leading to the overexpression of several cytokines. Moreover, the -/+ isoform speciffically caused the upregulation of fibrotic markers and the rearrangement of the actin cytoskeleton. Interestingly, the expression of the mesothelial marker UPK3B increased following the induction of the -/+ isoform. Because the expression of the -/+ variant led to the most signifficant isoform-specific changes in both cell lines, I focused on this isoform for the validation of the transcriptomic data of the IMCD3 cells. I confirmed that the induction of WT1 -/+ in the IMCD3 cells leads to the upregulation of fibrotic markers, increases cell adhesion and activates the AKT and MAPK pathways. Moreover, there was a…

Subjects/Keywords: 616.99; roles of WT1 isoforms; WT1; epithelial to mesenchymal transition; EMT

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Petrovich, G. (2016). Investigating the differential instructive roles of WT1's isoforms. (Doctoral Dissertation). University of Edinburgh. Retrieved from http://hdl.handle.net/1842/23423

Chicago Manual of Style (16^th Edition):

Petrovich, Giulia. “Investigating the differential instructive roles of WT1's isoforms.” 2016. Doctoral Dissertation, University of Edinburgh. Accessed April 10, 2021. http://hdl.handle.net/1842/23423.

MLA Handbook (7^th Edition):

Petrovich, Giulia. “Investigating the differential instructive roles of WT1's isoforms.” 2016. Web. 10 Apr 2021.

Vancouver:

Petrovich G. Investigating the differential instructive roles of WT1's isoforms. [Internet] [Doctoral dissertation]. University of Edinburgh; 2016. [cited 2021 Apr 10]. Available from: http://hdl.handle.net/1842/23423.

Council of Science Editors:

Petrovich G. Investigating the differential instructive roles of WT1's isoforms. [Doctoral Dissertation]. University of Edinburgh; 2016. Available from: http://hdl.handle.net/1842/23423

16. Limeta, Angelo. Tackling Metastatic Cancer: From Systems Biology to Therapeutics .

Degree: Chalmers tekniska högskola / Institutionen för biologi och bioteknik, 2019, Chalmers University of Technology

URL: http://hdl.handle.net/20.500.12380/300654

► Most cancer associated deaths are due to metastasis, the process in which a primary tumor migrates into neighboring tissues and forms secondary metastases. This project… (more)

Subjects/Keywords: Cancer; Metastasis; RNA-seq; Mesenchymal-to-Epithelial Transition; CRISPRCas13,; base editing

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Limeta, A. (2019). Tackling Metastatic Cancer: From Systems Biology to Therapeutics . (Thesis). Chalmers University of Technology. Retrieved from http://hdl.handle.net/20.500.12380/300654

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Limeta, Angelo. “Tackling Metastatic Cancer: From Systems Biology to Therapeutics .” 2019. Thesis, Chalmers University of Technology. Accessed April 10, 2021. http://hdl.handle.net/20.500.12380/300654.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Limeta, Angelo. “Tackling Metastatic Cancer: From Systems Biology to Therapeutics .” 2019. Web. 10 Apr 2021.

Vancouver:

Limeta A. Tackling Metastatic Cancer: From Systems Biology to Therapeutics . [Internet] [Thesis]. Chalmers University of Technology; 2019. [cited 2021 Apr 10]. Available from: http://hdl.handle.net/20.500.12380/300654.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Limeta A. Tackling Metastatic Cancer: From Systems Biology to Therapeutics . [Thesis]. Chalmers University of Technology; 2019. Available from: http://hdl.handle.net/20.500.12380/300654

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

17. García-Escolano, Marta. The inhibitor of differentiation genes expression and association with epithelial-to-mesenchymal markers in phenotypes of breast cancer: an in vitro and clinicopathological study .

Degree: 2019, University of Alicante

URL: http://hdl.handle.net/10045/113562

► Inhibitor of Differentiation (ID) proteins are a family of four (ID1-4) bHLH transcription factors that lack the DNA binding domain. They act by forming dimers… (more)

▼ Inhibitor of Differentiation (ID) proteins are a family of four (ID1-4) bHLH transcription factors that lack the DNA binding domain. They act by forming dimers with other transcriptional regulators and inhibiting their interaction with DNA. They play a crucial role during embryonic development and later in the adulthood, their expression is mostly restricted to a few populations of stem cells. In the last decades, many authors have described their re-activation and participation in tumor development, angiogenesis and EMT although the results are still controversial. In the first chapter of this research work, the role of ID genes as prognostic markers in breast cancer was evaluated. We studied the mRNA expression of the four ID genes and four markers of EMT by qRT-PCR in a clinical series of 307 primary breast carcinomas previously stratified in immunophenotypes. In addition, the expression of all these genes was measured in breast cancer cell lines and mammospheres. Overexpression of at least one ID gene was found in 48.9% of the studied samples. ID1 and ID4 were overexpressed mostly in TNBL and HER2-enriched subtypes, whereas ID2 and ID3 were overexpressed more frequently in luminal tumors. High ID1 and ID4 was associated with larger tumor size, histological grade 3, presence of necrosis and vascular invasion, and poorer outcome. Multivariate analysis revealed that ID4 and vascular invasion were independent factors for DFS. Regarding EMT markers, high levels of SNAI1 were associated with the overexpression of the four ID genes. Additionally, ID1 overexpression was positively related to TWIST1, and the overexpression of ID2 and ID3 was more frequently paired with tumors that conserve CHD1 expression. In vitro studies showed high expression of the four ID genes in all cell lines. However, when mammospheres were formed, mRNA levels of ID genes decreased, in contrast to SNAI1 and TWIST1, which mostly increased. In the second chapter of this thesis, we aimed to (a) describe the mechanisms of action of a small molecule pan-ID antagonist, (b) define its main targets and (c) investigate potential pathways of acquire resistance. Treatment with AGX51 led to Id protein loss, increase in ROS accumulation, cell cycle arrest, and cell death in all tumor cell lines tested. Here, we used an antioxidant compound in different cell lines to demonstrate that ROS are the main responsible of cell death following treatment with AGX51. A model of cultured quiescent cells not expressing ID proteins served to show that the main target of AGX51 are these proteins. Experiments with AGX-derivatives also supported these results. Finally, three mutagenizing agents were used in order to generate mutations that confer resistance to treatment with AGX51. Treatment with ENU gave rise to two clones apparently resistant to AGX51 effects. Based on our in vitro and clinicopathological studies, we conclude that ID1 and ID4 may act as biomarkers of worse prognosis in patients with breast cancer, and seem to be involved in the initiation of EMT mechanism.… Advisors/Committee Members: Peiró, Gloria (advisor).

Subjects/Keywords: Inhibitor of differentiation genes; Breast cancer; Epithelial to mesenchymal transition; Immunophenotype

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

García-Escolano, M. (2019). The inhibitor of differentiation genes expression and association with epithelial-to-mesenchymal markers in phenotypes of breast cancer: an in vitro and clinicopathological study . (Thesis). University of Alicante. Retrieved from http://hdl.handle.net/10045/113562

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

García-Escolano, Marta. “The inhibitor of differentiation genes expression and association with epithelial-to-mesenchymal markers in phenotypes of breast cancer: an in vitro and clinicopathological study .” 2019. Thesis, University of Alicante. Accessed April 10, 2021. http://hdl.handle.net/10045/113562.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

García-Escolano, Marta. “The inhibitor of differentiation genes expression and association with epithelial-to-mesenchymal markers in phenotypes of breast cancer: an in vitro and clinicopathological study .” 2019. Web. 10 Apr 2021.

Vancouver:

García-Escolano M. The inhibitor of differentiation genes expression and association with epithelial-to-mesenchymal markers in phenotypes of breast cancer: an in vitro and clinicopathological study . [Internet] [Thesis]. University of Alicante; 2019. [cited 2021 Apr 10]. Available from: http://hdl.handle.net/10045/113562.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

García-Escolano M. The inhibitor of differentiation genes expression and association with epithelial-to-mesenchymal markers in phenotypes of breast cancer: an in vitro and clinicopathological study . [Thesis]. University of Alicante; 2019. Available from: http://hdl.handle.net/10045/113562

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of California – Irvine

18. Villarreal Ponce, Alvaro P. An Ovol2-Zeb1 EMT-Regulatory Circuit Governs Mammary Basal-Luminal Binary Differentiation.

Degree: Biomedical Sciences, 2017, University of California – Irvine

URL: http://www.escholarship.org/uc/item/5b8693wg

► The capacity of epithelial cells to acquire enhanced lineage plasticity could depend on their ability to undergo EMT. Investigations performed on cultured epithelial cells support… (more)

▼ The capacity of epithelial cells to acquire enhanced lineage plasticity could depend on their ability to undergo EMT. Investigations performed on cultured epithelial cells support a link between EMT and bestowment of stem cell (SC)-like properties, raising the possibility that regulators of EMT may be responsible for producing an intermediate cellular identity between epithelial and mesenchymal states and is compatible with SC potential. The goal of my thesis project is to identify and characterize key transcriptional regulators of the dynamic EMT process that facilitate the production and maintenance of epithelial SCs, using the MG as a model system. The Dai laboratory identified Ovol2 as a TF that is required for mammary and epidermal development. My work contributed to the discovery of Ovol2 as a master negative regulator of EMT that directly represses the expression of various EMT-related genes, the most important being Zeb1, a critical mediator of Ovol2 loss-of-function effects. Zeb1 is a potent EMT-TF implicated in conferring SC-like traits to differentiated cells in mammary epithelial tumors. However, its in vivo role within normal mammary epithelia has not been studied. I found that Zeb1 also directly represses Ovol2, leading to the identification of an Ovol2-Zeb1 cross-repression circuit, which is shown by mathematic modeling to support intermediate cellular states between terminal epithelial and mesenchymal identities. Additionally, my data shows that Zeb1 expression is activated during early pregnancy in the basal cells of the mammary epithelium, which are known to gain multipotency upon pregnancy or transplantation. Using in vivo and ex vivo approaches to determine how perturbations to the Ovol2-Zeb1 circuit regulate stemness, I found this circuit to be important in modulating mammary SC basal-luminal differentiation. In addition to protecting basal cells from precocious differentiation toward a luminal fate, Zeb1 functions in regulating SC self-renewal/proliferative activity. Both mechanisms may contribute to the observed, Zeb1 loss-induced defect in ductal branching during mammary regeneration. My findings uncover a previously unknown role of Zeb1 and its associated molecular circuit in regulating mammary SC activity and basal/luminal differentiation, offering new insights into how epithelial plasticity contributes to stemness and identify novel transcriptional regulators of epithelial SCs.

Subjects/Keywords: Biology; Biochemistry; EMT; Epithelial Stem Cells; Epithelial-to-Mesenchymal Transition; Mammary gland; Ovol2; Zeb1

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Villarreal Ponce, A. P. (2017). An Ovol2-Zeb1 EMT-Regulatory Circuit Governs Mammary Basal-Luminal Binary Differentiation. (Thesis). University of California – Irvine. Retrieved from http://www.escholarship.org/uc/item/5b8693wg

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Villarreal Ponce, Alvaro P. “An Ovol2-Zeb1 EMT-Regulatory Circuit Governs Mammary Basal-Luminal Binary Differentiation.” 2017. Thesis, University of California – Irvine. Accessed April 10, 2021. http://www.escholarship.org/uc/item/5b8693wg.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Villarreal Ponce, Alvaro P. “An Ovol2-Zeb1 EMT-Regulatory Circuit Governs Mammary Basal-Luminal Binary Differentiation.” 2017. Web. 10 Apr 2021.

Vancouver:

Villarreal Ponce AP. An Ovol2-Zeb1 EMT-Regulatory Circuit Governs Mammary Basal-Luminal Binary Differentiation. [Internet] [Thesis]. University of California – Irvine; 2017. [cited 2021 Apr 10]. Available from: http://www.escholarship.org/uc/item/5b8693wg.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Villarreal Ponce AP. An Ovol2-Zeb1 EMT-Regulatory Circuit Governs Mammary Basal-Luminal Binary Differentiation. [Thesis]. University of California – Irvine; 2017. Available from: http://www.escholarship.org/uc/item/5b8693wg

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Washington

19. Rasmussen, Jeffrey Philip. Epithelial morphogenesis of the Caenorhabditis elegans pharynx.

Degree: PhD, 2012, University of Washington

URL: http://hdl.handle.net/1773/19742

► The assembly of cells into functional organs requires the coordination of cell shape and polarity with organ architecture. Although defects in cell shape and polarity… (more)

▼ The assembly of cells into functional organs requires the coordination of cell shape and polarity with organ architecture. Although defects in cell shape and polarity can lead to human disease, the in vivo regulation of these processes during organ formation is poorly understood. In this thesis, I used the Caenorhabditis elegans pharynx as an in vivo model to study organogenesis. Similar to many human organs, the pharynx is a tube formed from a monolayer of polarized epithelial cells that surround a central lumen. The pharyngeal lumen develops midway through embryogenesis when cells polarize along a central axis to form an epithelial cyst. Using live cell imaging, I found that cyst development is preceded by the grouping of pharyngeal precursors into a bilaterally symmetric intermediate. The organization of cells into this bilateral intermediate requires the POP-1/TCF cell fate pathway and the pharyngeal organ identity factor PHA-4/FoxA. Cyst formation begins when cells within the bilateral structure undergo a mesenchymal to epithelial transition and localize apical polarity determinants along their inner surfaces. These inner surfaces then constrict, creating the central lumen. I found that laminin, an integral basement membrane component, is required to define the axis of pharyngeal polarity. In laminin mutants, cells develop inverted polarity and constrict their outer surfaces, resulting in multiple pharyngeal lumens. After cyst formation, pharyngeal cells adopt highly reproducible morphologies. A previous ultrastructural study found that two cells, called pm8 and vpi1, develop into toroidally shaped single-cell tubes. By combining live cell microscopy with genetic analysis, I showed that pm8 and vpi1 form toroids via a novel mechanism: They wrap around the midline and then self-fuse, thereby creating an intracellular lumen. The self-fusion of pm8 and vpi1 into toroids requires fusogens and activation of the Notch signaling pathway in pm8. Thus, organogenesis of the pharynx requires sequential action of global, tissue-level signals, such as laminin, and local, cell-specific signals, such as Notch. Advisors/Committee Members: Priess, James R (advisor).

Subjects/Keywords: Caenorhabditis elegans; epithelial polarity; fusogen; laminin; mesenchymal to epithelial transition; tubulogenesis; Molecular and cellular biology

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Rasmussen, J. P. (2012). Epithelial morphogenesis of the Caenorhabditis elegans pharynx. (Doctoral Dissertation). University of Washington. Retrieved from http://hdl.handle.net/1773/19742

Chicago Manual of Style (16^th Edition):

Rasmussen, Jeffrey Philip. “Epithelial morphogenesis of the Caenorhabditis elegans pharynx.” 2012. Doctoral Dissertation, University of Washington. Accessed April 10, 2021. http://hdl.handle.net/1773/19742.

MLA Handbook (7^th Edition):

Rasmussen, Jeffrey Philip. “Epithelial morphogenesis of the Caenorhabditis elegans pharynx.” 2012. Web. 10 Apr 2021.

Vancouver:

Rasmussen JP. Epithelial morphogenesis of the Caenorhabditis elegans pharynx. [Internet] [Doctoral dissertation]. University of Washington; 2012. [cited 2021 Apr 10]. Available from: http://hdl.handle.net/1773/19742.

Council of Science Editors:

Rasmussen JP. Epithelial morphogenesis of the Caenorhabditis elegans pharynx. [Doctoral Dissertation]. University of Washington; 2012. Available from: http://hdl.handle.net/1773/19742

Universiteit Utrecht

20. Wiebrands, K. A role of epithelial-mesenchymal transitions in carcinogenic progression.

Degree: 2010, Universiteit Utrecht

URL: http://dspace.library.uu.nl:8080/handle/1874/190315

► The epithelial-mesenchymal transition plays an important role in several developmental processes, tissue repair, but is also associated with fibrosis and cancer. During tumorigenic progression, EMT… (more)

Subjects/Keywords: epithelial-mesenchymal transition; EMT; metastasis

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Wiebrands, K. (2010). A role of epithelial-mesenchymal transitions in carcinogenic progression. (Masters Thesis). Universiteit Utrecht. Retrieved from http://dspace.library.uu.nl:8080/handle/1874/190315

Chicago Manual of Style (16^th Edition):

Wiebrands, K. “A role of epithelial-mesenchymal transitions in carcinogenic progression.” 2010. Masters Thesis, Universiteit Utrecht. Accessed April 10, 2021. http://dspace.library.uu.nl:8080/handle/1874/190315.

MLA Handbook (7^th Edition):

Wiebrands, K. “A role of epithelial-mesenchymal transitions in carcinogenic progression.” 2010. Web. 10 Apr 2021.

Vancouver:

Wiebrands K. A role of epithelial-mesenchymal transitions in carcinogenic progression. [Internet] [Masters thesis]. Universiteit Utrecht; 2010. [cited 2021 Apr 10]. Available from: http://dspace.library.uu.nl:8080/handle/1874/190315.

Council of Science Editors:

Wiebrands K. A role of epithelial-mesenchymal transitions in carcinogenic progression. [Masters Thesis]. Universiteit Utrecht; 2010. Available from: http://dspace.library.uu.nl:8080/handle/1874/190315

21. Mourareau, Céline. Bio-CAD - Etude de biomarqueurs de progression tumorale dans les cancers des voies aéro-digestives supérieures en fonction de leur statut HPV. : Bio-CAD - Study of tumor progression biomarkers in upper aerodigestive tract cancers according to their HPV status.

Degree: Docteur es, Biologie céllulaire, 2016, Reims

URL: http://www.theses.fr/2016REIMS029

►

Chaque année 610 000 cancers sont diagnostiqués dans le monde induits par une infection à papillomavirus humains à haut-risque (HPV-HR). Bien que les carcinomes des… (more)

▼

Chaque année 610 000 cancers sont diagnostiqués dans le monde induits par une infection à papillomavirus humains à haut-risque (HPV-HR). Bien que les carcinomes des voies aéro-digestives supérieures (VADS) soient principalement associés à une forte consommation de tabac et d’alcool, 20 à 25% sont causés par une infection à HPV, particulièrement l’HPV de type 16. Les patients HPV positifs présentent un meilleur survi global, pourtant ils sont diagnostiqués avec plus de métastases à distance que les patients HPV négatifs. Au travers d’une étude sur des lignées cellulaires dérivées des VADS, nous avons montré que toutes les lignées cellulaires HPV+ présentaient une intégration du génome d’HPV au sein du génome cellulaire, avec des profils d’intégration différents. Les lignées pouvant être utilisées comme modèles caractéristiques des tumeurs HPV+ et HPV- sont respectivement les lignées UPCI:SCC090 et FaDu. La première par ses capacités migratoire et proliférative et la seconde par sa faible agressivité et une mutation du gène cellulaire p53. Dans une étude portant sur une série rétrospective de cancers de l’oropharynx éligible à une résection chirurgicale, 6 cancers sur 40 soit 15% présentaient une infection à HPV16 active (expression de l’ARNm E6*I). Nous avons étudié les marqueurs de TEM dans ces cancers oropharyngés en fonction du statut HPV. Nous avons retrouvé une perte plus importante du marqueur épithélial cadhérine-E au sein du groupe HPV+, associée à une moins bonne survie globale.Au total, nous montrons que le statut HPV et les marqueurs de TEM semblent être deux facteurs indépendants, qui peuvent se combiner pour définir des niveaux pronostiques différents.

Each year, 610,000 cancers are diagnosed worldwide attributed to high risk human papillomavirus (HR-HPV) infection. Although head and neck squamous cell carcinoma (HNSCC) is mainly associated with tobacco and/or alcohol consumption, 20 to 25% are caused by HPV infection, particularly HPV type 16. Although patients with HPV+ tumors present a better overall survival, they are diagnosed with more lymph node metastasis than HPV-negative patients.Through a study of HNSCC derived cell lines, we showed that all HPV-positives cell lines harbored HPV genome integration through host genome, with different integration profiles. Cell lines identified as good HPV+ and HPV- tumors models are UPCI:SCC090 and FaDu respectively. The first one by its migratory and proliferative properties, the second through its poor aggressiveness and mutation of p53 cellular gene.In a study on a retrospective series of oropharyngeal carcinomas with surgical resection, 6 out of 40 cancers shown HPV16 active infection (expressing E6*I mRNA). We studied epithelial-to-mesenchymal transition (EMT) markers on this oropharyngeal cancers, according to HPV status. We found a larger loss of epithelial marker E-cadherin in HPV+ group and loss of this marker is associated with a worse overall survival.We showed that HPV and EMT status seem to be two independent factors that could combine…

Advisors/Committee Members: Clavel, Christine (thesis director).

Subjects/Keywords: Carcinome; Oropharynx; Papillomavirus Humain; Transition Epithélio-Mésenchymateuse; Carcinoma; Oropharynx; Human Papillomavirus; Epithelial-To-Mesenchymal Transition

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Mourareau, C. (2016). Bio-CAD - Etude de biomarqueurs de progression tumorale dans les cancers des voies aéro-digestives supérieures en fonction de leur statut HPV. : Bio-CAD - Study of tumor progression biomarkers in upper aerodigestive tract cancers according to their HPV status. (Doctoral Dissertation). Reims. Retrieved from http://www.theses.fr/2016REIMS029

Chicago Manual of Style (16^th Edition):

Mourareau, Céline. “Bio-CAD - Etude de biomarqueurs de progression tumorale dans les cancers des voies aéro-digestives supérieures en fonction de leur statut HPV. : Bio-CAD - Study of tumor progression biomarkers in upper aerodigestive tract cancers according to their HPV status.” 2016. Doctoral Dissertation, Reims. Accessed April 10, 2021. http://www.theses.fr/2016REIMS029.

MLA Handbook (7^th Edition):

Mourareau, Céline. “Bio-CAD - Etude de biomarqueurs de progression tumorale dans les cancers des voies aéro-digestives supérieures en fonction de leur statut HPV. : Bio-CAD - Study of tumor progression biomarkers in upper aerodigestive tract cancers according to their HPV status.” 2016. Web. 10 Apr 2021.

Vancouver:

Mourareau C. Bio-CAD - Etude de biomarqueurs de progression tumorale dans les cancers des voies aéro-digestives supérieures en fonction de leur statut HPV. : Bio-CAD - Study of tumor progression biomarkers in upper aerodigestive tract cancers according to their HPV status. [Internet] [Doctoral dissertation]. Reims; 2016. [cited 2021 Apr 10]. Available from: http://www.theses.fr/2016REIMS029.

Council of Science Editors:

Mourareau C. Bio-CAD - Etude de biomarqueurs de progression tumorale dans les cancers des voies aéro-digestives supérieures en fonction de leur statut HPV. : Bio-CAD - Study of tumor progression biomarkers in upper aerodigestive tract cancers according to their HPV status. [Doctoral Dissertation]. Reims; 2016. Available from: http://www.theses.fr/2016REIMS029

22. Molina-Castro, Silvia. Study of the Hippo/YAP1 signaling pathway in gastric carcinogenesis induced by Helicobacter pylori : Etude de la voie de signalisation HIPPO/YAP dans la carcinogenèse gastrique induite par l'infection à Helicobacter pylori.

Degree: Docteur es, Microbiologie Immunologie, 2017, Bordeaux

URL: http://www.theses.fr/2017BORD0623

► Le cancer gastrique (CG) est une maladie multifactorielle, fréquemment associée à l’infection chronique par des souches CagA+ d’Helicobacter pylori. La transition épithélio-mésenchymateuse (EMT) est un… (more)

▼ Le cancer gastrique (CG) est une maladie multifactorielle, fréquemment associée à l’infection chronique par des souches CagA+ d’Helicobacter pylori. La transition épithélio-mésenchymateuse (EMT) est un processus réversible dans lequel une cellule épithéliale polarisée acquiert un phénotype mésenchymateux. L’EMT est à l’émergence de cellules souches cancéreuses (CSC) qui expriment CD44 et présentent une activité ALDH élevée. L’infection des cellules épithéliales gastriques humaines (CEGs) par CagA+ H. pylori induit des cellules CD44+ avec des propriétés des CSCs via une EMT. La voie Hippo est composée par les kinases MST et LATS, et leurs cibles, les YAP1 et TAZ. Suite à la phosphorylation, YAP1 et TAZ sont inhibés. YAP1 et TAZ activés lient les facteurs TEAD pour promouvoir la croissance cellulaire et l’inhibition de l’apoptose.Notre premier objectif était de rechercher si H. pylori change l’état d’activation de la voie Hippo et l'effet sur l’EMT et les CSC in vitro et in vivo. Le deuxième but est la caractérisation du rôle de YAP1/TEAD dans les propriétés de CSCs gastriques in vitro et les conséquences de son inhibition dans la croissance tumorale in vivo.Pour étudier la régulation de la voie Hippo pendant l’infection par H. pylori, LATS2, YAP1 et CD44 ont été évalués dans la muqueuse gastrique de sujets non-infectés et infectés par H. pylori, qui ont été augmentés avec l’infection et leur surexpression a été associée avec la gastrite et la métaplasie intestinale. Dans les CEGs l’expression de gènes de la voie Hippo a été altérée par l’infection. La régulation de la voie Hippo par H. pylori a une cinétique diphasique et dépendante de CagA. Dans l’infection précoce, H. pylori déclenche l’activité transcriptionelle de YAP1. Cette période d’inactivité de la voie Hippo est suivi de son activation progressive, soutenue par l’accumulation de LATS2 et la phosphorylation inhibitrice de YAP1. La répression de LATS2 avec siRNAs a accéléré l’acquisition du phénotype mésenchymateux après l’infection, l’augmentation de marqueurs de l’EMT (Zeb1 et Snail1), et la diminution des miR-200 épithéliaux. Les CSC induites par H. pylori ont été potentialisées par l’inhibition de LATS2, ce qui suggère que LATS2 limite l’EMT et le phénotype de CSC acquis pendant l’infection. L’inhibition de LATS2 ou YAP1 diminue l’expression de ces deux protéines, révélant ainsi une boucle de régulation positive. Dans des coupes de tissu de CG, l’expression de LATS2 et YAP1 est hétérogène et positivement corrélée, fait qui a été confirmé dans 38 CEGs de la CCLE. L’expression LATS2 est fortement corrélée à celle de CTGF et CYR61, ce qui suggère que LATS2 peut aussi être un gène cible de YAP1/TEAD.La verteporfine (VP) est capable d’interrompre l’interaction YAP1/TEAD, et donc d’inhiber son activité transcriptionelle. In vitro, utilisant CEGs et des cellules de tumeurs de patients amplifiées chez la souris (patient-derived xenograft PDX), le traitement à la VP a diminué la croissance cellulaire, l’expression de gènes cible de YAP1/TAZ/TEAD, l’activité du… Advisors/Committee Members: Varon, Christine (thesis director).

Subjects/Keywords: Cellules souches gastriques; Transition épithélio-mésenchymateuse; CD44; Cancer stem cells; Epithelial to mesenchymal transition; CD44

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Molina-Castro, S. (2017). Study of the Hippo/YAP1 signaling pathway in gastric carcinogenesis induced by Helicobacter pylori : Etude de la voie de signalisation HIPPO/YAP dans la carcinogenèse gastrique induite par l'infection à Helicobacter pylori. (Doctoral Dissertation). Bordeaux. Retrieved from http://www.theses.fr/2017BORD0623

Chicago Manual of Style (16^th Edition):

Molina-Castro, Silvia. “Study of the Hippo/YAP1 signaling pathway in gastric carcinogenesis induced by Helicobacter pylori : Etude de la voie de signalisation HIPPO/YAP dans la carcinogenèse gastrique induite par l'infection à Helicobacter pylori.” 2017. Doctoral Dissertation, Bordeaux. Accessed April 10, 2021. http://www.theses.fr/2017BORD0623.

MLA Handbook (7^th Edition):

Molina-Castro, Silvia. “Study of the Hippo/YAP1 signaling pathway in gastric carcinogenesis induced by Helicobacter pylori : Etude de la voie de signalisation HIPPO/YAP dans la carcinogenèse gastrique induite par l'infection à Helicobacter pylori.” 2017. Web. 10 Apr 2021.

Vancouver:

Molina-Castro S. Study of the Hippo/YAP1 signaling pathway in gastric carcinogenesis induced by Helicobacter pylori : Etude de la voie de signalisation HIPPO/YAP dans la carcinogenèse gastrique induite par l'infection à Helicobacter pylori. [Internet] [Doctoral dissertation]. Bordeaux; 2017. [cited 2021 Apr 10]. Available from: http://www.theses.fr/2017BORD0623.

Council of Science Editors:

Molina-Castro S. Study of the Hippo/YAP1 signaling pathway in gastric carcinogenesis induced by Helicobacter pylori : Etude de la voie de signalisation HIPPO/YAP dans la carcinogenèse gastrique induite par l'infection à Helicobacter pylori. [Doctoral Dissertation]. Bordeaux; 2017. Available from: http://www.theses.fr/2017BORD0623

University of Vienna

23. Martinez Turtos, Adriana. Extracellular vesicles and their impact on the epithelial plasticity of hepatocellular carcinoma cells.

Degree: 2018, University of Vienna

URL: http://othes.univie.ac.at/51143/

► Leberkrebs ist der weltweit sechsthäufigste maligne Tumor, der zur zweithäufigsten Mortalität aller Krebserkrankten führt. Das hepatozelluläre Karzinom (HCC) ist der vorherrschende primäre Leberkrebs. Die schlechte… (more)

▼ Leberkrebs ist der weltweit sechsthäufigste maligne Tumor, der zur zweithäufigsten Mortalität aller Krebserkrankten führt. Das hepatozelluläre Karzinom (HCC) ist der vorherrschende primäre Leberkrebs. Die schlechte Prognose von HCC Patienten ist mit fehlenden Biomarkern für die diagnostische Früherkennung sowie einer häufig auftretenden Metastasierung nach chirurgischer Entfernung des Primärtumors begründet. Darum sind geeignete Diagnosen und Therapien für die erfolgreiche Bekämpfung des HCC von äußerster Wichtigkeit. Tumor-abgeleitete Exosomen sind kleine extrazelluläre Vesikel (sEVs), die von Tumoren produziert werden und diese in vielen ihrer Entwicklungsstadien beeinflussen und regulieren können. Kürzliche Studien haben gezeigt, dass metastasierende HCC Zellen sEVs freisetzen können, welche die Migration und Invasivität von differenzierten Hepatozyten mittels eines epithelial zu mesenchymalen Transition (EMT)-ähnlichen Prozesses induzieren. Das Verständnis der sEV Funktionen in der metastatischen Kaskade des HCC könnte die Basis für die Entwicklung einer neuen zielgerichteten Therapie sein. In dieser Studie wurden differenzierte HepG2 Zellen verwendet, um herauszufinden, ob sEVs von EMT- transformierten HCC Zellen einen Einfluss auf die Zellplastizität von epithelialen Zellen haben. Die, von mesenchymalen HCC Zellen gewonnen, EVs konnten eine Veränderung der epithelialen Zellplastizität der HepG2 Zellen durch Verminderung der E-Cadherin Expression induzieren. Die reduzierte E-Cadherin Expression war unabhängig von einer verstärkten Abundanz mesenchymaler Marker oder charakteristischen EMT-Transkriptionsfaktoren. Die für das Experiment verwendeten EVs wurden vorab bezüglich ihrer Größe und EV- spezifischer Marker charakterisiert. Zudem wurde der Anteil der sEVs innerhalb der EV Population mittels Nanopartikelanalyse bestimmt. Die durch differentielle Ultrazentrifugation (DUC) gewonnene sEV–Fraktion betrug über 50%. Kommerziell erhältliche Kits, die auf Membranaffinität basieren, zeigten eine geringere sEV Ausbeute verglichen mit der DUC- Methode. Western Blot Analysen der DUC isolierten EVs ergaben eine Anreicherung mit den Tetraspanin-Proteinen CD63 und CD81 sowie das Vorhandensein von TSG101 und das Fehlen des Endoplasmatischen-Reticulum Proteins GRP78. Zusätzlich wurden CD63-GFP exprimierende HCC Zelllinien für die Freisetzung von GFP-markierten sEVs generiert, die für weiterführende in vivo Untersuchungen zur Funktion einer prämetastatischen Nische eingesetzt werden sollen. CD63-GFP markierte EVs wurden mittels Immunfluoreszenzmikroskopie, Western Blot Analyse und Durchflusszytometrie nachgewiesen und einzelne Zellklone selektiert. In diesen Experimenten soll der Effekt von EVs auf die Ausbildung einer prämetastatischen Nische nach Xenotransplantation in immundefizienten Mäusen geklärt werden. Zusammenfassend zeigt diese Studie die Rolle von EVs als Vermittler in der Zell-Zell Kommunikation zwischen mesenchymalen und epithelialen HCC Zellen auf. Es konnte gezeigt werden, dass EVs von mesenchymalen Zellen eine…

Subjects/Keywords: 42.13 Molekularbiologie; hepatozelluläre Karzinom / epithelial zu mesenchymalen Transition / extrazelluläre Vesikel; hepatocellular carcinoma / epithelial-to-mesenchymal transition / extracellular vesicles

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Martinez Turtos, A. (2018). Extracellular vesicles and their impact on the epithelial plasticity of hepatocellular carcinoma cells. (Thesis). University of Vienna. Retrieved from http://othes.univie.ac.at/51143/

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Martinez Turtos, Adriana. “Extracellular vesicles and their impact on the epithelial plasticity of hepatocellular carcinoma cells.” 2018. Thesis, University of Vienna. Accessed April 10, 2021. http://othes.univie.ac.at/51143/.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Martinez Turtos, Adriana. “Extracellular vesicles and their impact on the epithelial plasticity of hepatocellular carcinoma cells.” 2018. Web. 10 Apr 2021.

Vancouver:

Martinez Turtos A. Extracellular vesicles and their impact on the epithelial plasticity of hepatocellular carcinoma cells. [Internet] [Thesis]. University of Vienna; 2018. [cited 2021 Apr 10]. Available from: http://othes.univie.ac.at/51143/.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Martinez Turtos A. Extracellular vesicles and their impact on the epithelial plasticity of hepatocellular carcinoma cells. [Thesis]. University of Vienna; 2018. Available from: http://othes.univie.ac.at/51143/

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

24. Carter, Lauren. Defining the Epithelial-to-Mesenchymal Transition and Regulation of Stemness in the Ovarian Surface Epithelium .

Degree: 2018, University of Ottawa

URL: http://hdl.handle.net/10393/38491

► The ovarian surface epithelium (OSE) is a monolayer of cells surrounding the ovary that is ruptured during ovulation. After ovulation the wound is repaired, however… (more)

▼ The ovarian surface epithelium (OSE) is a monolayer of cells surrounding the ovary that is ruptured during ovulation. After ovulation the wound is repaired, however this process, and the mechanisms to maintain OSE homeostasis after the wound is repaired are poorly understood. We have shown the mouse OSE (mOSE) contains a stem cell population that is expanded by Transforming Growth Factor Beta 1 (TGFB1), a factor present in follicular fluid. These data suggest that components in the follicular fluid such as TGFB1 may promote wound repair and OSE homeostasis through maintenance of the OSE stem cell population. Additionally, TGFB1 may promote wound repair through induction of an epithelial-to-mesenchymal transition (EMT) and activation of pro-survival pathways, as seen in other tissues. To elucidate the mechanism for TGFB1-mediated ovulatory wound repair, mOSE cells were treated with TGFB1, which induced an EMT seen with increased Snai1 expression and cell migration. Snai1 overexpression also increased cell migration and sphere formation (a stem cell characteristic). RNA sequencing results suggest this is at least in part through elevated collagen deposition in SNAI1 overexpressing cells. A TGFB signalling targets array identified Cox2 induction following TGFB1 treatment. Constitutive Cox2 expression did not promote an EMT, but enhanced sphere formation and cell survival. Finally, TGFB1 treatment decreased Brca1 expression, which when deleted from mOSE cells also increased sphere formation. RNA sequencing results suggest that Brca1 deletion promotes stemness through activation of the stem cell genes Ly6a and Lgr5. RNA sequencing was also used to compare mOSE cells cultured as monolayers and as spheroids, with and without TGFB1. These results validate our findings that TGFB1 promotes an EMT partially through Snail induction and the upregulation of Cox2. mOSE cells cultured as spheroids acquire a mesenchymal transcriptional profile that is further enhanced with TGFB1 treatment. These data suggest that TGFB1 may promote ovulatory wound repair and maintain OSE homeostasis through the induction of an EMT, maintenance of the stem cell population and activation of a pro-survival pathway. Interestingly, mOSE spheroids also decrease Brca1 expression and upregulate cancer associated genes such as Pax8 and Greb1. The induction of survival pathways, while simultaneously increasing stemness and repressing Brca1 could render cells more susceptible to transformation. This work provides novel insights as to why ovulation is the primary non-hereditary risk factor for ovarian cancer.

Subjects/Keywords: ovarian surface epithelium; ovulation; stemness; epithelial-to-mesenchymal transition; wound repair; Cox2; Brca1; Snai1

10 more images…

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Carter, L. (2018). Defining the Epithelial-to-Mesenchymal Transition and Regulation of Stemness in the Ovarian Surface Epithelium . (Thesis). University of Ottawa. Retrieved from http://hdl.handle.net/10393/38491

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Carter, Lauren. “Defining the Epithelial-to-Mesenchymal Transition and Regulation of Stemness in the Ovarian Surface Epithelium .” 2018. Thesis, University of Ottawa. Accessed April 10, 2021. http://hdl.handle.net/10393/38491.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Carter, Lauren. “Defining the Epithelial-to-Mesenchymal Transition and Regulation of Stemness in the Ovarian Surface Epithelium .” 2018. Web. 10 Apr 2021.

Vancouver:

Carter L. Defining the Epithelial-to-Mesenchymal Transition and Regulation of Stemness in the Ovarian Surface Epithelium . [Internet] [Thesis]. University of Ottawa; 2018. [cited 2021 Apr 10]. Available from: http://hdl.handle.net/10393/38491.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Carter L. Defining the Epithelial-to-Mesenchymal Transition and Regulation of Stemness in the Ovarian Surface Epithelium . [Thesis]. University of Ottawa; 2018. Available from: http://hdl.handle.net/10393/38491

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Tulane University

25. Hoang, Van. Differential regulation of the EMT axis by MEK1/2 and MEK5 in triple-negative breast cancer.

Degree: 2016, Tulane University

URL: https://digitallibrary.tulane.edu/islandora/object/tulane:74409

►

Triple-negative breast cancer (TNBC) presents a clinical challenge due to the aggressive nature of the disease and a lack of targeted therapies. Constitutive activation of… (more)

▼

Triple-negative breast cancer (TNBC) presents a clinical challenge due to the aggressive nature of the disease and a lack of targeted therapies. Constitutive activation of the mitogen-activated protein kinase (MAPK)/extracellular signal-regulated kinase (ERK) pathway has been linked to chemoresistance and metastatic progression through distinct mechanisms, including activation of epithelial-to-mesenchymal transition (EMT) whereby cells adopt a motile and invasive phenotype through loss of epithelial markers, namely Cadherin 1/E-Cadherin (CDH1), and acquisition of mesenchymal markers, such as vimentin (VIM) and Cadherin 2/N-Cadherin (CDH2). While MAPK/ERK1/2 kinase inhibitors (MEKi) have shown promise as antitumor agents in the preclinical setting, application has had limited success clinically. Activation of compensatory signaling, potentially contributing to the emergence of drug resistance, has shifted the therapeutic strategy to combine MEK1/2 inhibitors with agents targeting oncoproteins (RAF) or parallel growth pathways (PI3K). Conventional MAPK family members have been well-characterized in modulation of cellular processes involved in tumor initiation and progression, yet the role of MEK5-ERK5 in cancer biology is not completely understood. Recent studies have highlighted the importance of the MEK5 pathway in metastatic progression of various cancer types, including those of the prostate, colon, bone and breast. Furthermore, elevated levels of ERK5 expression and activity observed in breast carcinomas are linked to worse prognosis in TNBC patients. The purpose of this work is to explore MEK5 regulation of the EMT axis and to evaluate a novel pan-MEK inhibitor on clinically aggressive TNBC cells. Our results show a distinction between the MEK1/2 and MEK5 cascades in maintenance of the mesenchymal phenotype, suggesting that the MEK5 pathway may be necessary and sufficient in EMT regulation while MEK1/2 signaling further sustains the mesenchymal state of TNBC cells. Furthermore, additive effects on MET induction are evident through the inhibition of both MEK1/2 and MEK5. Taken together, these data demonstrate the need for a better understanding of the individual roles of MEK1/2 and MEK5 signaling in breast cancer and provide rationale for combined targeting of these pathways to circumvent compensatory signaling and subsequent therapeutic resistance.

1

Van Hoang

Advisors/Committee Members: Burow, Matthew (Thesis advisor), School of Medicine Biomedical Sciences Graduate Program (Degree granting institution).

Subjects/Keywords: MAPK signaling (MEK1/2, MEK5); triple-negative breast cancer (TNBC); epithelial-to-mesenchymal transition (EMT)

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Hoang, V. (2016). Differential regulation of the EMT axis by MEK1/2 and MEK5 in triple-negative breast cancer. (Thesis). Tulane University. Retrieved from https://digitallibrary.tulane.edu/islandora/object/tulane:74409

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Hoang, Van. “Differential regulation of the EMT axis by MEK1/2 and MEK5 in triple-negative breast cancer.” 2016. Thesis, Tulane University. Accessed April 10, 2021. https://digitallibrary.tulane.edu/islandora/object/tulane:74409.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Hoang, Van. “Differential regulation of the EMT axis by MEK1/2 and MEK5 in triple-negative breast cancer.” 2016. Web. 10 Apr 2021.

Vancouver:

Hoang V. Differential regulation of the EMT axis by MEK1/2 and MEK5 in triple-negative breast cancer. [Internet] [Thesis]. Tulane University; 2016. [cited 2021 Apr 10]. Available from: https://digitallibrary.tulane.edu/islandora/object/tulane:74409.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Hoang V. Differential regulation of the EMT axis by MEK1/2 and MEK5 in triple-negative breast cancer. [Thesis]. Tulane University; 2016. Available from: https://digitallibrary.tulane.edu/islandora/object/tulane:74409

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

26. Akrida, Ioanna. Μελέτη σηματοδοτικών οδών που εμπλέκονται στην επιθηλιο-μεσεγχυματική μετατροπή στους φυλλοειδείς όγκους μαστού.

Degree: 2018, University of Patras; Πανεπιστήμιο Πατρών

URL: http://hdl.handle.net/10442/hedi/45271

►

Phyllodes breast tumors (PTs) are rare fibroepithelial neoplasms, currently classified as benign, borderline and malignant. PTs can recur locally and may have metastatic potential. They… (more)

▼

Phyllodes breast tumors (PTs) are rare fibroepithelial neoplasms, currently classified as benign, borderline and malignant. PTs can recur locally and may have metastatic potential. They are biphasic neoplasms consisting of epithelial and stromal components, therefore they can serve as an excellent model of epithelial-stromal interactions in vivo. Epithelial-mesenchymal transition (EMT) is a phenotypic conversion that takes place in physiological processes such as embryogenesis and wound healing, as well as in fibrotic diseases and cancer. There is an emerging theory that EMT contributes to tumor progression not only by facilitating migration and invasion, but also by generating cells with a hybrid phenotype and properties of stemness, evasion of apoptosis and chemoresistance. In this study, we aimed to investigate the expression of multiple EMT associated factors in relation to tumor grade in phyllodes breast tumors. Materials and Methods: Immunohistochemical expression of the epithelial marker E-cadherin, the dual functio n protein β-catenin involved in cell adhesion and Wnt signaling as well, the mesenchymal markers vimentin and N-cadherin, the EMT activating transcription factors ZEB1, Snail1, Twist1 and the ΕΜΤ inducer integrin linked kinase (ILK) was evaluated in 96 FFPE human phyllodes breast tumors [48/96 (50%) benign, 27/96 (28,1%) borderline and 21/96 (21,9%) malignant]. Results: An EMT-associated immunohistochemical expression profile consisting of decreased membranous and increased nuclear/cytoplasmic immunopositivity of E-cadherin and β-catenin, as well as increased expression of N-cadherin, vimentin, Snail1, ZEB1 and Twist1 was detected in both the epithelial and the stromal tumor cells, and significantly correlated to advanced tumor grade. Cytoplasmic and nuclear immunoreactivity of ILK was observed in the epithelial and the stromal component of phyllodes breast tumors and was significantly higher in borderline/malignant tumors. We found a significant correlation of ILK expression with all of the EMT markers examined. Conclusion: The program of EMT is activated in phyllodes breast tumors and is related to tumor grade, thus contributing to tumor progression. ILK is also implicated in the pathogenesis of borderline/malignant phyllodes tumors and probably exerts its tumor-promoting action through an EMT-mediated mechanism. To the best of our knowledge, this is the first report of the role of ZEB1 and ILK in phyllodes breast tumors pathogenesis.

Οι φυλλοειδείς όγκοι του μαστού είναι σπάνια ινοεπιθηαλικά νεοπλάσματα με ικανότητα τοπικής υποτροπής και δυναμικό μετάστασης, και ταξινομούνται με βάση ιστολογικά κριτήρια σε καλοήθεις, οριακής κακοήθειας και κακοήθεις. Είναι διφασικοί όγκοι που αποτελούνται από επιθηλιακό και από στρωματικό στοιχείο και επομένως αποτελούν άριστο μοντέλο μελέτης των αλληλεπιδράσεων επιθηλιακών και μεσεγχυματικών κυττάρων in vivo. Η επιθηλιομεσεγχυματική μετατροπή (ΕΜΤ), ένα κυτταρικό πρόγραμμα μέσω του οποίου τα επιθηλιακά κύτταρα αποκτούν μεσεγχυματικό φαινότυπο,…

Subjects/Keywords: Επιθηλιομεσενχυματική μετατροπή (ΕΜΤ); Φυλλοειδείς όγκοι μαστού; Epithelial to mesenchymal transition; Phyllodes breast tumors

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Akrida, I. (2018). Μελέτη σηματοδοτικών οδών που εμπλέκονται στην επιθηλιο-μεσεγχυματική μετατροπή στους φυλλοειδείς όγκους μαστού. (Thesis). University of Patras; Πανεπιστήμιο Πατρών. Retrieved from http://hdl.handle.net/10442/hedi/45271

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Akrida, Ioanna. “Μελέτη σηματοδοτικών οδών που εμπλέκονται στην επιθηλιο-μεσεγχυματική μετατροπή στους φυλλοειδείς όγκους μαστού.” 2018. Thesis, University of Patras; Πανεπιστήμιο Πατρών. Accessed April 10, 2021. http://hdl.handle.net/10442/hedi/45271.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Akrida, Ioanna. “Μελέτη σηματοδοτικών οδών που εμπλέκονται στην επιθηλιο-μεσεγχυματική μετατροπή στους φυλλοειδείς όγκους μαστού.” 2018. Web. 10 Apr 2021.

Vancouver:

Akrida I. Μελέτη σηματοδοτικών οδών που εμπλέκονται στην επιθηλιο-μεσεγχυματική μετατροπή στους φυλλοειδείς όγκους μαστού. [Internet] [Thesis]. University of Patras; Πανεπιστήμιο Πατρών; 2018. [cited 2021 Apr 10]. Available from: http://hdl.handle.net/10442/hedi/45271.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Akrida I. Μελέτη σηματοδοτικών οδών που εμπλέκονται στην επιθηλιο-μεσεγχυματική μετατροπή στους φυλλοειδείς όγκους μαστού. [Thesis]. University of Patras; Πανεπιστήμιο Πατρών; 2018. Available from: http://hdl.handle.net/10442/hedi/45271

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Penn State University

27. Wokpetah, Joseph Mawumenyo. Regulation of cancer stem cells by the tumor microenvironment.

Degree: 2014, Penn State University

URL: https://submit-etda.libraries.psu.edu/catalog/21336

► Cancer is the abnormal growth of cells that tend to multiply in an uncontrolled way and, in some cases, metastasize to other locations in the… (more)

Subjects/Keywords: Epithelial to mesenchymal transition; metastasis; transforming growth factor beta; Young's modulus; upregulation; downregulation

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Wokpetah, J. M. (2014). Regulation of cancer stem cells by the tumor microenvironment. (Thesis). Penn State University. Retrieved from https://submit-etda.libraries.psu.edu/catalog/21336

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Wokpetah, Joseph Mawumenyo. “Regulation of cancer stem cells by the tumor microenvironment.” 2014. Thesis, Penn State University. Accessed April 10, 2021. https://submit-etda.libraries.psu.edu/catalog/21336.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Wokpetah, Joseph Mawumenyo. “Regulation of cancer stem cells by the tumor microenvironment.” 2014. Web. 10 Apr 2021.

Vancouver:

Wokpetah JM. Regulation of cancer stem cells by the tumor microenvironment. [Internet] [Thesis]. Penn State University; 2014. [cited 2021 Apr 10]. Available from: https://submit-etda.libraries.psu.edu/catalog/21336.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Wokpetah JM. Regulation of cancer stem cells by the tumor microenvironment. [Thesis]. Penn State University; 2014. Available from: https://submit-etda.libraries.psu.edu/catalog/21336

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

28. G. Celesti. MESENCHYMAL FEATURES MEDIATED BY TWIST1 IN COLORECTAL CANCER CELLS AND MICROENVIRONMENT.

Degree: 2011, Università degli Studi di Milano

URL: http://hdl.handle.net/2434/158084

► Background. Colorectal cancer (CRC) is a major cause of death for cancer in western countries, ranking third in both sexes. Therapeutic developments in the past… (more)

▼ Background. Colorectal cancer (CRC) is a major cause of death for cancer in western countries, ranking third in both sexes. Therapeutic developments in the past decades have extended life expectancy in patients with advanced disease (i.e., stage III), and even for those with distant metastasis (i.e., stage IV). Most treatments for advanced disease nowadays include a combination of chemotherapy with target therapy. Despite advances, the fact that metastatic colorectal cancer remains largely incurable, pushes to pursue a better understanding of the factors underlying cancer progression. Nowadays, a major field of investigation is the relationship between epithelial tumor cells and the surrounding compartment, namely tumor microenvironment, and in particular its contribution to cancer progression. The tumor microenvironment essentially comprises tumor infiltrating cells, vasculature, extracellular matrix, plus other matrix associated molecules. Transformed cells can modulate the functions of stromal cells, likely to facilitate their own growth and survival. In this Darwinian perspective, outgrowth of cancer cells goes together with local changes. Such changes, like clonal ones, are likely progressive, from the stage of local invasion, up to regional lymph-node colonization and finally to the development of distant metastasis. Infiltrating cells are a mix of populations having myeloid or mesenchymal origin, including tumor-associated macrophages, myeloid -derived suppressor cells, mast cells, monocytes, neutrophils, CD3+ T cells, natural killers, dendritic cells, endothelial cells, mesenchymal stem cells and cancer-associated fibroblasts. Taken together, all these players are involved in a double-faced game, in which an anti-tumor effect (such as that exerted by CD3+ cells in early CRC, [1]) is counteracted by a cancer promoting one (e.g., that exerted by macrophages [2]. Currently, this cancer-microenvironment match implies contradictory and controversial data, largely depending upon the investigated cell population and upon the experimental setting. This Ariadnes' thread seems unravelled, mainly because of the contemporaneous evolution of both tumor and microenvironment cells during multi-stage tumor progression. What is certainly perceived today, is that a switch from a genetic to a non-clonal prospective is required to understand tumor evolution. Clearly, the dynamic architecture of the stromal compartment and the interactions therein, need to be reconciled with the evidences concerning genetic irreversible changes in stromal cells. The latter include loss of heterozygosis, microsatellite instability (MSI) [3], trisomy of Chromosome 7 in connective tissues elements of CRC [4], and p53 mutations (in the stroma of breast carcinoma[5]). These surprising results rise the possibility that the stromal compartment contains not only an admixture of non-neoplastic cells, but also cancer cells with an aggressive and invasive phenotype which became able to invade the surrounding tissues by mimicking fibroblast morphology.… Advisors/Committee Members: tutore: Massimo Roncalli, correlatore: Luigi Laghi, RONCALLI, MASSIMO.

Subjects/Keywords: epithelial to mesenchymal transition; colorectal cancer; metastasis; twist1; Settore BIO/10 - Biochimica

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Celesti, G. (2011). MESENCHYMAL FEATURES MEDIATED BY TWIST1 IN COLORECTAL CANCER CELLS AND MICROENVIRONMENT. (Thesis). Università degli Studi di Milano. Retrieved from http://hdl.handle.net/2434/158084

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Celesti, G.. “MESENCHYMAL FEATURES MEDIATED BY TWIST1 IN COLORECTAL CANCER CELLS AND MICROENVIRONMENT.” 2011. Thesis, Università degli Studi di Milano. Accessed April 10, 2021. http://hdl.handle.net/2434/158084.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Celesti, G.. “MESENCHYMAL FEATURES MEDIATED BY TWIST1 IN COLORECTAL CANCER CELLS AND MICROENVIRONMENT.” 2011. Web. 10 Apr 2021.

Vancouver:

Celesti G. MESENCHYMAL FEATURES MEDIATED BY TWIST1 IN COLORECTAL CANCER CELLS AND MICROENVIRONMENT. [Internet] [Thesis]. Università degli Studi di Milano; 2011. [cited 2021 Apr 10]. Available from: http://hdl.handle.net/2434/158084.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Celesti G. MESENCHYMAL FEATURES MEDIATED BY TWIST1 IN COLORECTAL CANCER CELLS AND MICROENVIRONMENT. [Thesis]. Università degli Studi di Milano; 2011. Available from: http://hdl.handle.net/2434/158084

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Wayne State University

29. Maitah, Ma'in Yehya. Hedgehog signaling: a potential therapeutic target for non-small cell lung cancer.

Degree: PhD, Pathology, 2011, Wayne State University

URL: https://digitalcommons.wayne.edu/oa_dissertations/320

► The American Cancer Society estimated that 222,520 Americans were diagnosed with lung cancer and 157,300 died of lung cancer in 2010 (Jemal et al.… (more)

▼ The American Cancer Society estimated that 222,520 Americans were diagnosed with lung cancer and 157,300 died of lung cancer in 2010 (Jemal et al. 2009, 225-249;Jemal et al. 2011, 69-90). The clinical outcome of patients diagnosed with non-small cell lung cancer (NSCLC), the major lung cancer sub-types, is very poor, which calls for innovative research for finding novel therapeutic targets and agents for better treatment outcome. Emerging evidences have suggested that a phenomenon called Epithelial-to-Mesenchymal Transition (EMT), which shares similar molecular characteristics with cancer stem-like cells, contributes to lung cancer treatment failure. In view of the fact that EMT process has been implicated in the two important biological processes that are accountable for cancer-related deaths; the progression of cancer cells to a distant organ, and the acquisition of resistance to conventional cancer therapeutics (Leng et al. 2011, 145-155;Shih and Yang 2011;Zhang et al. 2011), needs further in-depth investigation. Therefore, further mechanistic understanding of the role of EMT in lung cancer is very important, which was the focus of my investigation. In this study, I found for the first time that the induction of EMT by chronic exposure of A549 NSCLC cells to TGF-Β1 (A549-M cells) led to the up-regulation of sonic hedgehog (Shh) both at the mRNA and protein levels causing activation of hedgehog signaling. These results were also reproduced in another NSCLC cell line (H2030), and these results were further associated with the induction of EMT phenotype. Induction of EMT was found to be consistent with aggressive characteristics such as increased clonogenic growth, cell motility and invasion. The aggressiveness of these cells was attenuated by the treatment of A549-M cells with pharmacological inhibitors of Hh signaling in addition to Shh knock-down by siRNA. The inhibition of Hh signaling by pharmacological inhibitors led to the reversal of EMT phenotype as confirmed by the reduction of mesenchymal markers such as ZEB1 and Fibronectin, and induction of epithelial marker E-cadherin. In addition, knock-down of Shh by siRNA significantly attenuated EMT induction by TGF-Β1. Next, I examined the involvement of NF-κB, as downstream of TGF-Β-receptor signaling, and in the up-regulation of Shh. I tested whether NF-κB activity could indeed be induced by TGF-Β1 in our model cell culture system. To gain further mechanistic insight, I also tested whether the active NF-κB could bind to consensus sequences on Shh promoter in cell free system. Additionally, I determined the binding of the active NF-κB to Shh promoter in the cell by CHIP assay. Finally, I evaluated whether NF-κB can activate Shh expression directly using Shh promoter-luciferase reporter assays. The results clearly showed that TGF-Β1 induced NF-κB activity in NSCLC cell line A549. In addition, active NF-κB bound to its consensus sequences in the Shh promoter. Likewise, on CHIP assay, I found that active NF-κB… Advisors/Committee Members: Fazlul H. Sarkar.

Subjects/Keywords: Cancer; Epithelial to mesenchymal transition; Lung Cancer; Sonic Hedgehog; TGF-beta; Molecular Biology; Oncology; Pharmacology

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Maitah, M. Y. (2011). Hedgehog signaling: a potential therapeutic target for non-small cell lung cancer. (Doctoral Dissertation). Wayne State University. Retrieved from https://digitalcommons.wayne.edu/oa_dissertations/320

Chicago Manual of Style (16^th Edition):

Maitah, Ma'in Yehya. “Hedgehog signaling: a potential therapeutic target for non-small cell lung cancer.” 2011. Doctoral Dissertation, Wayne State University. Accessed April 10, 2021. https://digitalcommons.wayne.edu/oa_dissertations/320.

MLA Handbook (7^th Edition):

Maitah, Ma'in Yehya. “Hedgehog signaling: a potential therapeutic target for non-small cell lung cancer.” 2011. Web. 10 Apr 2021.

Vancouver:

Maitah MY. Hedgehog signaling: a potential therapeutic target for non-small cell lung cancer. [Internet] [Doctoral dissertation]. Wayne State University; 2011. [cited 2021 Apr 10]. Available from: https://digitalcommons.wayne.edu/oa_dissertations/320.

Council of Science Editors:

Maitah MY. Hedgehog signaling: a potential therapeutic target for non-small cell lung cancer. [Doctoral Dissertation]. Wayne State University; 2011. Available from: https://digitalcommons.wayne.edu/oa_dissertations/320

Washington State University

30. [No author]. Mechanisms of Endometrial Regeneration .

Degree: 2013, Washington State University

URL: http://hdl.handle.net/2376/4771

► The uterus is one of the most plastic adult organs with tremendous regenerative capacity. The endometrium (innermost lining of the uterus) undergoes regular cycles of… (more)

▼ The uterus is one of the most plastic adult organs with tremendous regenerative capacity. The endometrium (innermost lining of the uterus) undergoes regular cycles of remodeling by transitioning through stages of growth, differentiation, degeneration and regeneration. Remodeling and regeneration of the endometrium occur during pregnancy and following parturition in all mammalian species. Mechanisms coordinating regeneration of the endometrium during the menstrual/estrous cycle and following parturition are poorly understood. Hypothesized mechanisms include proliferation/migration of residual epithelium, cellular transdifferentiation, engraftment of bone marrow-derived cells and contribution of endometrial stem/progenitor cells. Herein, experiments were designed to determine the contributions of cellular transdifferentiation (i.e., mesenchymal-to-epithelial transition; MET), residual glandular epithelium (GE) and stem/progenitor cells to regeneration using mouse models. In the first study, in vivo fate-mapping and characterization of epithelial-mesenchymal transitional cells revealed a role for MET in endometrial regeneration. In the second study, temporal regenerative changes were assessed in regards to glandular GE and efforts were made to identify signaling factors that direct endometrial regeneration. It was determined that GE likely contributes to re-epithelialization of the lumen and the regenerative process is not dependent on estrogen receptor alpha, but rather, relies on paracrine signaling. The third study demonstrated the use of histone H2B-GFP label-retaining transgenic mice as a method to enrich for endometrial stem/progenitor cells. Most importantly, in the fourth study a novel model for transplantation into regenerating uteri was developed to determine the presence and function of candidate endometrial stem/progenitor cells. This model will serve as an invaluable tool for identifying endometrial stem/progenitor cells and evaluating their functional contributions to regeneration, homeostasis and pregnancy. It is reasoned that a more complete understanding of the complex mechanisms of endometrial regeneration will provide insight into how these processes may contribute to uterine disease and infertility when not properly regulated. Advisors/Committee Members: Pru, James (advisor).

Subjects/Keywords: Biology; Endometrial regeneration; Endometrium; Mesenchymal-to-epithelial transition; Stem Cells; Transdifferentiation; Uterus

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

author], [. (2013). Mechanisms of Endometrial Regeneration . (Thesis). Washington State University. Retrieved from http://hdl.handle.net/2376/4771

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

author], [No. “Mechanisms of Endometrial Regeneration .” 2013. Thesis, Washington State University. Accessed April 10, 2021. http://hdl.handle.net/2376/4771.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

author], [No. “Mechanisms of Endometrial Regeneration .” 2013. Web. 10 Apr 2021.

Vancouver:

author] [. Mechanisms of Endometrial Regeneration . [Internet] [Thesis]. Washington State University; 2013. [cited 2021 Apr 10]. Available from: http://hdl.handle.net/2376/4771.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

author] [. Mechanisms of Endometrial Regeneration . [Thesis]. Washington State University; 2013. Available from: http://hdl.handle.net/2376/4771

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

		in
And / Or
		in
And / Or
		in
And / Or
		in

Open Access Theses and Dissertations