subject:(mammary epithelial cells)

Massey University

1. Biet, Juliane. Effect of mechanical stress o the integrity, signalling mechanisms and function of bovine mammary epithelial cells : a thesis submitted in partial fulfilment of the requirements for the degree of Doctor of Philosophy in Animal Science at Massey University, Manawatū, Palmerston North, New Zealand .

Degree: 2014, Massey University

URL: http://hdl.handle.net/10179/7214

► Mammary gland engorgement due to milk accumulation in late lactation leads to changes in cell morphology and has been recognised as a potential key initiator… (more)

▼ Mammary gland engorgement due to milk accumulation in late lactation leads to changes in cell morphology and has been recognised as a potential key initiator of involution and remodelling of the mammary gland. The physical distension of mammary epithelial cells (MEC), due to udder filling, is likely to result in mechanical tension on cell-cell and cell-matrix interactions. Cell-cell and cellmatrix junctions provide tissue integrity, promote cell polarity, guarantee sufficient communication between cells to ensure synchronised milk secretion and support cell survival. Their disruption may be one of the early initiators of the mammary gland remodelling process. As a consequence, the primary goal of this study was to determine the potential effects of MEC stretch on changes in cell sensing within the mechanical micro-environment in the initiation of bovine MEC involution. During this investigation, particular emphasis was put on three potential mechanosensors: tight junctions (TJ), focal adhesions (FA) and primary cilia (PC), and their regulation in the early stages of involution using in vivo and in vitro experimental approaches. Static, biaxial in vitro cell stretch and acute physical distension in vivo resulted in changes in TJ protein expression levels implying a potential disruption of cell-cell communication as well as communication with the cell‟s cytoskeleton. Furthermore, down-regulation of Akt and pAkt following different periods of mechanical strain applied in vitro and decreased levels of pAkt following acute physical distension in vivo indicated a disruption of β1-integrin-FAK survival signalling through the PI3K-Akt pathway downstream of FA interactions. Increased numbers of ciliated MEC following extended periods of non-milking indicated a dedifferentiation of MEC. Furthermore, increased levels of STAT6 transcription (part of PC signalling following mechanical stimulation) factor indicates the initiation of macrophage accumulation and promotion of tissue remodelling of the bovine mammary gland. In conclusion, this study supports the hypothesis that local factors play an important role during bovine mammary gland involution and that mechanical stimulation may play a part in the initiation of this process.

Subjects/Keywords: Mammary glands; Epithelial cells; Bovine mammary glands

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APA (6^th Edition):

Biet, J. (2014). Effect of mechanical stress o the integrity, signalling mechanisms and function of bovine mammary epithelial cells : a thesis submitted in partial fulfilment of the requirements for the degree of Doctor of Philosophy in Animal Science at Massey University, Manawatū, Palmerston North, New Zealand . (Thesis). Massey University. Retrieved from http://hdl.handle.net/10179/7214

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):

Biet, Juliane. “Effect of mechanical stress o the integrity, signalling mechanisms and function of bovine mammary epithelial cells : a thesis submitted in partial fulfilment of the requirements for the degree of Doctor of Philosophy in Animal Science at Massey University, Manawatū, Palmerston North, New Zealand .” 2014. Thesis, Massey University. Accessed March 03, 2021. http://hdl.handle.net/10179/7214.

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

MLA Handbook (7^th Edition):

Biet, Juliane. “Effect of mechanical stress o the integrity, signalling mechanisms and function of bovine mammary epithelial cells : a thesis submitted in partial fulfilment of the requirements for the degree of Doctor of Philosophy in Animal Science at Massey University, Manawatū, Palmerston North, New Zealand .” 2014. Web. 03 Mar 2021.

Vancouver:

Biet J. Effect of mechanical stress o the integrity, signalling mechanisms and function of bovine mammary epithelial cells : a thesis submitted in partial fulfilment of the requirements for the degree of Doctor of Philosophy in Animal Science at Massey University, Manawatū, Palmerston North, New Zealand . [Internet] [Thesis]. Massey University; 2014. [cited 2021 Mar 03]. Available from: http://hdl.handle.net/10179/7214.

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

Council of Science Editors:

Biet J. Effect of mechanical stress o the integrity, signalling mechanisms and function of bovine mammary epithelial cells : a thesis submitted in partial fulfilment of the requirements for the degree of Doctor of Philosophy in Animal Science at Massey University, Manawatū, Palmerston North, New Zealand . [Thesis]. Massey University; 2014. Available from: http://hdl.handle.net/10179/7214

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

2. Moreno Layseca, Paulina. The role of β1-integrin in normal and oncogene-mediated proliferation in breast epithelia.

Degree: PhD, 2015, University of Manchester

URL: https://www.research.manchester.ac.uk/portal/en/theses/the-role-of-1integrin-in-normal-and-oncogenemediated-proliferation-in-breast-epithelia(635388a7-5382-4cb5-82d1-d098b2092e2e).html ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.634970

► Luminal epithelial cells in the mammary gland require two types of signals to proliferate: soluble signals (growth factor signals) and signals from the extracellular matrix… (more)

▼ Luminal epithelial cells in the mammary gland require two types of signals to proliferate: soluble signals (growth factor signals) and signals from the extracellular matrix (ECM). The composition of the ECM is sensed by adhesion receptors such as integrins. Integrins modulate cell behaviour and play a key role in cell cycle entry. Altered integrin expression and signalling has been associated with breast cancer and studies using mouse mammary epithelial cells (MECs) have shown that the absence of β1-integrin induces growth arrest. However, it is not completely understood how integrins transduce the signals from the plasma membrane to the nucleus to induce cell cycle entry. Thus, the first aim of this project was to determine how β1-integrin controls proliferation in MECs. I established a model to study the effects of depleting β1-integrin using the FSK7 mammary epithelial cell line. The proliferation defect observed in this β1-integrin knockdown model was rescued by expressing a constitutively active Rac1 or Pak. Moreover, inhibiting Rac1 or Pak prevented normal proliferation in MECs in a similar fashion as β1-integrin depletion. Furthermore, in this thesis I have identified the complex comprised of Src, paxillin and p130Cas as a potential link between β1-integrin and Rac1. These results provide an insight into the mechanism that regulates proliferation downstream of β1-integrin. During breast cancer initiation, β1-integrin signals are disrupted. This indicates that additional signals must be driving proliferation during tumorigenesis. Therefore, the second aim of this project was to test whether expression of breast oncogenes can overcome the proliferation defect present in β1-integrin null cells. In order to do so, an oncogenic ErbB2, a constitutively active form of Akt (myrAkt) and the Notch1 intracellular domain (NICD) were transfected in the β1-integrin knockdown MECs. The results showed that ErbB2 overcomes the need for β1-integrin by signalling to Pak. NICD does not require β1-integrin to drive proliferation by an unknown mechanism. Expression of myrAkt did not restore normal levels of proliferation in β1-integrin depleted MECs. This finding suggests that Akt is not sufficient to induce cell cycle entry by itself and instead, both Akt and Erk signalling are needed to exert this function. This work has further delineated the specific signals controlling proliferation downstream of β1-integrin, and has provided a model to test the dependence of oncogenes for β1-integrin to drive proliferation in MECs. These studies are important to understand the role of β1-integrin in breast cancer formation and to define the types of breast cancer where β1-integrin can be used as an effective therapeutic target.

Subjects/Keywords: 611; Integrins; Proliferation; Mammary epithelial cells

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APA (6^th Edition):

Moreno Layseca, P. (2015). The role of β1-integrin in normal and oncogene-mediated proliferation in breast epithelia. (Doctoral Dissertation). University of Manchester. Retrieved from https://www.research.manchester.ac.uk/portal/en/theses/the-role-of-1integrin-in-normal-and-oncogenemediated-proliferation-in-breast-epithelia(635388a7-5382-4cb5-82d1-d098b2092e2e).html ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.634970

Chicago Manual of Style (16^th Edition):

Moreno Layseca, Paulina. “The role of β1-integrin in normal and oncogene-mediated proliferation in breast epithelia.” 2015. Doctoral Dissertation, University of Manchester. Accessed March 03, 2021. https://www.research.manchester.ac.uk/portal/en/theses/the-role-of-1integrin-in-normal-and-oncogenemediated-proliferation-in-breast-epithelia(635388a7-5382-4cb5-82d1-d098b2092e2e).html ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.634970.

MLA Handbook (7^th Edition):

Moreno Layseca, Paulina. “The role of β1-integrin in normal and oncogene-mediated proliferation in breast epithelia.” 2015. Web. 03 Mar 2021.

Vancouver:

Moreno Layseca P. The role of β1-integrin in normal and oncogene-mediated proliferation in breast epithelia. [Internet] [Doctoral dissertation]. University of Manchester; 2015. [cited 2021 Mar 03]. Available from: https://www.research.manchester.ac.uk/portal/en/theses/the-role-of-1integrin-in-normal-and-oncogenemediated-proliferation-in-breast-epithelia(635388a7-5382-4cb5-82d1-d098b2092e2e).html ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.634970.

Council of Science Editors:

Moreno Layseca P. The role of β1-integrin in normal and oncogene-mediated proliferation in breast epithelia. [Doctoral Dissertation]. University of Manchester; 2015. Available from: https://www.research.manchester.ac.uk/portal/en/theses/the-role-of-1integrin-in-normal-and-oncogenemediated-proliferation-in-breast-epithelia(635388a7-5382-4cb5-82d1-d098b2092e2e).html ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.634970

Queens University

3. Apostoli, Anthony J. The Mammary Epithelial Contribution Of PPARγ In Breast Tumourigenesis .

Degree: Pathology and Molecular Medicine, 2014, Queens University

URL: http://hdl.handle.net/1974/12347

► Previous studies with peroxisome proliferator-activated receptor (PPAR)γ heterozygous mice suggest PPARγ normally suppresses 7,12-dimethylbenz[a]anthracene (DMBA)-induced breast tumour progression, but the mechanisms and cell types involved… (more)

Subjects/Keywords: Knockout Mouse Model ; Chemical Carcinogenesis ; Breast cancer ; Mammary Epithelial Cells ; Mammary Secretory Epithelial Cells ; PPARγ

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APA (6^th Edition):

Apostoli, A. J. (2014). The Mammary Epithelial Contribution Of PPARγ In Breast Tumourigenesis . (Thesis). Queens University. Retrieved from http://hdl.handle.net/1974/12347

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):

Apostoli, Anthony J. “The Mammary Epithelial Contribution Of PPARγ In Breast Tumourigenesis .” 2014. Thesis, Queens University. Accessed March 03, 2021. http://hdl.handle.net/1974/12347.

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

MLA Handbook (7^th Edition):

Apostoli, Anthony J. “The Mammary Epithelial Contribution Of PPARγ In Breast Tumourigenesis .” 2014. Web. 03 Mar 2021.

Vancouver:

Apostoli AJ. The Mammary Epithelial Contribution Of PPARγ In Breast Tumourigenesis . [Internet] [Thesis]. Queens University; 2014. [cited 2021 Mar 03]. Available from: http://hdl.handle.net/1974/12347.

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

Council of Science Editors:

Apostoli AJ. The Mammary Epithelial Contribution Of PPARγ In Breast Tumourigenesis . [Thesis]. Queens University; 2014. Available from: http://hdl.handle.net/1974/12347

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

University of Connecticut

4. Procopio, Maria L, Ms. The Expression of T-Box (Tbx3) in the Bovine Mammary Gland.

Degree: MS, Animal Science, 2011, University of Connecticut

URL: https://opencommons.uconn.edu/gs_theses/143

► Development of the bovine mammary gland is a complex process that is regulated by several hormones, growth factors and transcription factors including but not… (more)

Subjects/Keywords: Mammary epithelial cells; mammary fibroblasts; transcription factors; Growth Hormone; Insulin-Like Growth Factor-I

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APA (6^th Edition):

Procopio, Maria L, M. (2011). The Expression of T-Box (Tbx3) in the Bovine Mammary Gland. (Masters Thesis). University of Connecticut. Retrieved from https://opencommons.uconn.edu/gs_theses/143

Chicago Manual of Style (16^th Edition):

Procopio, Maria L, Ms. “The Expression of T-Box (Tbx3) in the Bovine Mammary Gland.” 2011. Masters Thesis, University of Connecticut. Accessed March 03, 2021. https://opencommons.uconn.edu/gs_theses/143.

MLA Handbook (7^th Edition):

Procopio, Maria L, Ms. “The Expression of T-Box (Tbx3) in the Bovine Mammary Gland.” 2011. Web. 03 Mar 2021.

Vancouver:

Procopio, Maria L M. The Expression of T-Box (Tbx3) in the Bovine Mammary Gland. [Internet] [Masters thesis]. University of Connecticut; 2011. [cited 2021 Mar 03]. Available from: https://opencommons.uconn.edu/gs_theses/143.

Council of Science Editors:

Procopio, Maria L M. The Expression of T-Box (Tbx3) in the Bovine Mammary Gland. [Masters Thesis]. University of Connecticut; 2011. Available from: https://opencommons.uconn.edu/gs_theses/143

University of Maryland

5. Choudhary, Ratan Kumar. Identification and characterization of presumptive bovine mammary stem cells.

Degree: Animal Sciences, 2011, University of Maryland

URL: http://hdl.handle.net/1903/12521

► An understanding of the characteristics and regulation of mammary stem cells (MaSCs) is needed to gain insight into normal gland development and carcinogenesis. Previous profiling… (more)

▼ An understanding of the characteristics and regulation of mammary stem cells (MaSCs) is needed to gain insight into normal gland development and carcinogenesis. Previous profiling of MaSCs relied upon immunophenotypic selection of enzymatically dispersed cells by flow cytometry. However, these approaches involved the selection of cells that are removed from their tissue location and cellular microenvironment. In this study, I have utilized an alternative approach called laser microdissection, to excise putative MaSCs, based upon their ability to retain bromodeoxyuridine labeled DNA for an extended period, and control cells from their in situ locations in prepubertal bovine mammary cryosections. First, I established a protocol to immunostain putative MaSCs in tissue cryosections and isolate RNA of high quality. Next, I excised putative MaSCs and control cells from immunostained cryosections using laser microdissection. Global gene expression analysis by microarray provided evidence that MaSCs were located in the basal epithelium and progenitor cells located in suprabasal layers. A number of genes that were up-regulated in MaSCs and progenitor cells were identified and these are potential biomarkers. Analysis of the expression pattern of four genes (NR5A2, NUP153, HNF4A and FNDC3B) by immunohistochemistry showed that the protein expression profile was consistent with microarray data. Detailed immunohistochemical analyses of NR5A2, NUP153, HNF4A and FNDC3B in calf and cows (at various stages of lactation) revealed that their frequency and distribution were consistent with stem/progenitor cell characteristics. Finally, I attempted to manipulate stem/progenitor cells number using cultures of primary mammary epithelial cells. Expansion of stem/progenitor cell is a prerequisite for stem cell therapeutics and facilitates stem cell research. The effect of xanthosine on bovine mammary epithelial cells (MEC) was evaluated. The result of this study showed that xanthosine treatment increased cell proliferation, promoted symmetric cell division and increased expression of telomerase and a novel stem cell marker (FNDC3B). Together, these studies identified novel, potential markers for MaSCs and progenitor cells, and supported the ability of xanthosine to increase stem/progenitor cell number. Advisors/Committee Members: Capuco, Anthony V (advisor), Mather, Ian H (advisor).

Subjects/Keywords: Animal sciences; Laser microdissection; Mammary stem cell; Microarray; Primary mammary epithelial cells; Xanthosine

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

APA (6^th Edition):

Choudhary, R. K. (2011). Identification and characterization of presumptive bovine mammary stem cells. (Thesis). University of Maryland. Retrieved from http://hdl.handle.net/1903/12521

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):

Choudhary, Ratan Kumar. “Identification and characterization of presumptive bovine mammary stem cells.” 2011. Thesis, University of Maryland. Accessed March 03, 2021. http://hdl.handle.net/1903/12521.

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

MLA Handbook (7^th Edition):

Choudhary, Ratan Kumar. “Identification and characterization of presumptive bovine mammary stem cells.” 2011. Web. 03 Mar 2021.

Vancouver:

Choudhary RK. Identification and characterization of presumptive bovine mammary stem cells. [Internet] [Thesis]. University of Maryland; 2011. [cited 2021 Mar 03]. Available from: http://hdl.handle.net/1903/12521.

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

Council of Science Editors:

Choudhary RK. Identification and characterization of presumptive bovine mammary stem cells. [Thesis]. University of Maryland; 2011. Available from: http://hdl.handle.net/1903/12521

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

University of California – Irvine

6. 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

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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 March 03, 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. 03 Mar 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 Mar 03]. 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

Deakin University

7. Freestone David. Copper homeostasis in human mammary epithelial cells.

Degree: School of Life and Environmental Sciences, 2013, Deakin University

URL: http://hdl.handle.net/10536/DRO/DU:30056796

Adequate amounts of copper in milk are critical for normal neonatal development, however the mechanisms regulating copper supply to milk have not been clearly defined. This thesis analysed copper transporting proteins in mammary epithelial cells and the impact of copper and lactational hormones upon the regulation these proteins was measured.

Subjects/Keywords: Copper homeostasis; Human mammary epithelial cells; Copper transporting proteins

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APA (6^th Edition):

David, F. (2013). Copper homeostasis in human mammary epithelial cells. (Thesis). Deakin University. Retrieved from http://hdl.handle.net/10536/DRO/DU:30056796

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):

David, Freestone. “Copper homeostasis in human mammary epithelial cells.” 2013. Thesis, Deakin University. Accessed March 03, 2021. http://hdl.handle.net/10536/DRO/DU:30056796.

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

MLA Handbook (7^th Edition):

David, Freestone. “Copper homeostasis in human mammary epithelial cells.” 2013. Web. 03 Mar 2021.

Vancouver:

David F. Copper homeostasis in human mammary epithelial cells. [Internet] [Thesis]. Deakin University; 2013. [cited 2021 Mar 03]. Available from: http://hdl.handle.net/10536/DRO/DU:30056796.

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

Council of Science Editors:

David F. Copper homeostasis in human mammary epithelial cells. [Thesis]. Deakin University; 2013. Available from: http://hdl.handle.net/10536/DRO/DU:30056796

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

University of Glasgow

8. Song, Hyuk. A mutagenic study of functional and structural aspects of rat insulin-like growth factor binding protein-5.

Degree: PhD, 2001, University of Glasgow

URL: http://theses.gla.ac.uk/76135/ ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.341987

► On going research in our laboratory is focussed on the potential role of Insulin-like growth factor binding protein-5 (IGFBP-5) in apoptosis of mammary epithelial cells.… (more)

▼ On going research in our laboratory is focussed on the potential role of Insulin-like growth factor binding protein-5 (IGFBP-5) in apoptosis of mammary epithelial cells. In order to increase our understanding of IGFBP-5 functions, the work described below focussed on the relationship between the structure of the binding protein and its important molecular interactions. Using site-directed mutagenesis, we have mutated two highly conserved amino acids, Gly203 and Gln209 (G203K and Q209A respectively) within the basic amino acid rich region (201- 218) in the C-terminal domain of rat IGFBP-5. After analysis of binding activity using three different methods - IGF ligand blotting, IGF solution phase equilibrium binding and biosensor measurement - we have shown that the mutation of either of these two residues results in a reduction in affinity of the binding protein for both IGF-I and IGF-II by approximately ten-fold. Furthermore, mutation of both amino acids (G203K/Q209A, termed the Double mutant) had a cumulative effect and results in the complete ablation of IGF-I binding and a several thousand-fold reduction in IGF-II binding. This reduction in IGF binding affinity was comparable to that observed for the C-terminally truncated mutant BP550 (residues 1-168), which suggests that Gly203 and Gln209 may be the major determinants for IGF binding in the C-terminal domain. In addition, using heparin ligand blots, we confirm that mutation of basic residues within the C-terminal 201- 218 region (Hep- mutant: R201L, K202E, K206Q and R214A) results in major attenuation of heparin binding, whereas the G203K and Q209A single mutants and the Double mutant have no reduction in heparin binding. Therefore, our data suggests a potential overlap of heparin- and IGF- binding domains in the C-terminal region of IGFBP-5, and based on this, we discuss a potential model to explain the observed lower IGF binding affinity of ECM-bound IGFBP-5. In an attempt to assess the separate contribution of the N- and C-terminal domains to IGF binding, we also made four chimeric IGFBP cDNAs, BP552, BP522, BP255 and BP225, by switching domains between rat IGFBP-5 and rat IGFBP-2. We were consistently unable to detect expression of BP225 protein in the baculovirus/insect cell system, so this chimera had to be excluded from further study. Recognition of BP552 and BP522 proteins by both anti-rat IGFBP-5 and anti-rat IGFBP-2 antisera confirms their identity as chimeric proteins made up of domains from the native binding proteins, while BP255 was only recognised by the anti-rat IGFBP-5. The IGF binding properties of unpurified BP552, BP522 and BP255 proteins were assessed by IGF ligand blotting and IGF solution phase binding assays. These experiments demonstrated that BP552 and BP522 had comparable affinities with native IGFBP, whereas we were unable to detect any binding of BP255 to IGF-I by either technique, and only very weak interaction with IGF-II. Purified BP552 and BP522 were also tested by biosensor analysis, and data confirmed the results from the…

Subjects/Keywords: 572.8; Apoptosis; Mammary epithelial cells

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

APA (6^th Edition):

Song, H. (2001). A mutagenic study of functional and structural aspects of rat insulin-like growth factor binding protein-5. (Doctoral Dissertation). University of Glasgow. Retrieved from http://theses.gla.ac.uk/76135/ ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.341987

Chicago Manual of Style (16^th Edition):

Song, Hyuk. “A mutagenic study of functional and structural aspects of rat insulin-like growth factor binding protein-5.” 2001. Doctoral Dissertation, University of Glasgow. Accessed March 03, 2021. http://theses.gla.ac.uk/76135/ ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.341987.

MLA Handbook (7^th Edition):

Song, Hyuk. “A mutagenic study of functional and structural aspects of rat insulin-like growth factor binding protein-5.” 2001. Web. 03 Mar 2021.

Vancouver:

Song H. A mutagenic study of functional and structural aspects of rat insulin-like growth factor binding protein-5. [Internet] [Doctoral dissertation]. University of Glasgow; 2001. [cited 2021 Mar 03]. Available from: http://theses.gla.ac.uk/76135/ ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.341987.

Council of Science Editors:

Song H. A mutagenic study of functional and structural aspects of rat insulin-like growth factor binding protein-5. [Doctoral Dissertation]. University of Glasgow; 2001. Available from: http://theses.gla.ac.uk/76135/ ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.341987

Massey University

9. Cooper Phyn, Claire Vanessa. Regulation of tight junction proteins during engorgement of the mammary gland.

Degree: PhD, Animal Science, 2006, Massey University

URL: http://hdl.handle.net/10179/1572

► Extended periods of milk accumulation result in loss of secretory activity, increased apoptosis and eventually, involution of mammary glands. This process is associated with increased… (more)

▼ Extended periods of milk accumulation result in loss of secretory activity, increased apoptosis and eventually, involution of mammary glands. This process is associated with increased permeability of the tight junction (TJ) complexes between adjacent mammary epithelial cells (MECs). The change in cell shape during mammary engorgement from a cuboidal to a flattened morphology may initiate changes in protein and gene expression (mechanotransduction) that trigger these processes. Therefore, this study examined the regulation of the major TJ protein components during mammary engorgement, and in particular the role of physical distension of the mammary epithelium in the regulatory process. Expression of the integral transmembrane TJ proteins, occludin and claudin-1, and the cytoplasmic TJ protein, ZO-1, were down-regulated in both bovine and rat mammary glands during the early stages of mammary apoptosis and involution following the abrupt cessation of milk removal. In the rat, these responses were locally regulated as they occurred only in teat-sealed glands in a hemi-suckled model. Furthermore, the down-regulation of TJ proteins is consistent with a loss of TJ integrity during mammary engorgement. Induced physical distension of rat mammary glands in vivo transiently up-regulated the expression levels of occludin protein and mRNA, and ZO-1 mRNA, followed by an accelerated decrease in expression compared with the effects of milk accumulation alone. This was associated with the initiation of apoptosis, the up-regulation of the pro-apoptotic factor pSTAT3, and the down-regulation of the cell-ECM survival factor βl-integrin. An in vitro model was also developed to stretch MECs, mimicking the flattening in cell shape during mammary engorgement in vivo. While stretching MECs in vitro did not conclusively alter TJ protein expression, the overall results of this project support further investigation into the role of the TJ complex in mechanotransduction pathways. In addition, the results point to crosstalk between cell-ECM survival signalling and STAT3 death signalling as a candidate for regulation by physical distension of the mammary epithelium. In conclusion, this study supports the hypothesis that physical distension during engorgement of the mammary glands with milk is a primary trigger initiating apoptosis of MECs through changes in the regulation of gene pathways controlling cell survival and death, and the disruption of TJ function.

Subjects/Keywords: Mammary epithelial cells; Apoptosis

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APA (6^th Edition):

Cooper Phyn, C. V. (2006). Regulation of tight junction proteins during engorgement of the mammary gland. (Doctoral Dissertation). Massey University. Retrieved from http://hdl.handle.net/10179/1572

Chicago Manual of Style (16^th Edition):

Cooper Phyn, Claire Vanessa. “Regulation of tight junction proteins during engorgement of the mammary gland.” 2006. Doctoral Dissertation, Massey University. Accessed March 03, 2021. http://hdl.handle.net/10179/1572.

MLA Handbook (7^th Edition):

Cooper Phyn, Claire Vanessa. “Regulation of tight junction proteins during engorgement of the mammary gland.” 2006. Web. 03 Mar 2021.

Vancouver:

Cooper Phyn CV. Regulation of tight junction proteins during engorgement of the mammary gland. [Internet] [Doctoral dissertation]. Massey University; 2006. [cited 2021 Mar 03]. Available from: http://hdl.handle.net/10179/1572.

Council of Science Editors:

Cooper Phyn CV. Regulation of tight junction proteins during engorgement of the mammary gland. [Doctoral Dissertation]. Massey University; 2006. Available from: http://hdl.handle.net/10179/1572

University of Georgia

10. Williams, Jarred Mathew. Presence of soluble CD14 in bovine and equine milk.

Degree: 2014, University of Georgia

URL: http://hdl.handle.net/10724/29352

► Soluble CD14 (sCD14) is a protein receptor specific for LPS, which circulates in the blood of many species, such as cows and horses. We showed… (more)

Subjects/Keywords: Colostrum; Soluble CD14; Bovine Mammary Epithelial Cells,; Endotoxin; Septicemia; Passive Immunity

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APA (6^th Edition):

Williams, J. M. (2014). Presence of soluble CD14 in bovine and equine milk. (Thesis). University of Georgia. Retrieved from http://hdl.handle.net/10724/29352

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):

Williams, Jarred Mathew. “Presence of soluble CD14 in bovine and equine milk.” 2014. Thesis, University of Georgia. Accessed March 03, 2021. http://hdl.handle.net/10724/29352.

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

MLA Handbook (7^th Edition):

Williams, Jarred Mathew. “Presence of soluble CD14 in bovine and equine milk.” 2014. Web. 03 Mar 2021.

Vancouver:

Williams JM. Presence of soluble CD14 in bovine and equine milk. [Internet] [Thesis]. University of Georgia; 2014. [cited 2021 Mar 03]. Available from: http://hdl.handle.net/10724/29352.

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

Council of Science Editors:

Williams JM. Presence of soluble CD14 in bovine and equine milk. [Thesis]. University of Georgia; 2014. Available from: http://hdl.handle.net/10724/29352

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

11. Mahbouli, Sinda. Etude de l'impact de la leptine sur le statut oxydatif et inflammatoire du tissu mammaire : approche expérimentale in vitro et in vivo - Mise en oeuvre de la technique de détection par fluorescence native. : Impact of leptin on oxidative and inflammatory status of the mammary tissue. An in-vitro and in- vivo experimental approach using the native fluorescence detection technique.

Degree: Docteur es, Sciences de la vie et de la sante, 2015, Clermont-Ferrand 1

URL: http://www.theses.fr/2015CLF1PP04

► La leptine est une hormone peptidique ayant une action sur de nombreux tissus. Une dérégulation de la sécrétion de cette hormone est observée au cours… (more)

▼ La leptine est une hormone peptidique ayant une action sur de nombreux tissus. Une dérégulation de la sécrétion de cette hormone est observée au cours de l’obésité. L’obésité est fréquemment associée à des troubles de santé dont les principaux sont le diabète de type II, l’hypertension artérielle et les maladies cardiovasculaires. Elle est également un facteur de risque du cancer du sein, particulièrement en post-ménopause favorisant la récidive et augmentant la mortalité. Ces perturbations, associées à un état de stress oxydant défini par un excès de production des espèces réactives de l’oxygène (ERO) par rapport aux systèmes de défense antioxydants, pourraient avoir un impact majeur dans le risque de carcinogenèse chez le sujet obèse. Il est clairement établi aujourd’hui que le statut oxydatif des cellules est directement corrélé aux capacités de prolifération mais aussi de survie des cellules dans leur environnement. A ce jour, très peu de données existent concernant le rôle de la leptine dans la modulation du statut oxydatif des cellules épithéliales mammaires saines et tumorales. L’objectif de cette thèse était d’étudier d'abord les mécanismes d’action et les effets de la leptine sur le statut oxydatif et inflammatoire des cellules épithéliales mammaires saines et néoplasiques ; puis dans un deuxième temps, une étude expérimentale a été conduite pour caractériser in vivo l’impact de l’obésité associée ou non à l’activité physique sur la croissance tumorale et le statut oxydatif et inflammatoire des tumeurs. Le projet avait également pour but de mettre en œuvre une nouvelle technique d’analyse basée sur la détection de fluorescence native induite par excitation laser à 224 nm afin d’évaluer la production de composés bio-actifs de la famille des éicosanoïdes, dont les isoprostanes, impliqués dans le processus inflammatoire. Nous avons exploré in vitro l’impact de la leptine sur le statut oxydatif des cellules épithéliales mammaires. Cette étude nous a permis d’établir que la réponse au signal leptinique varie en fonction du statut néoplasique de la lignée considérée, en fonction du temps de contact et non de la dose testée. Ensuite, nous avons étudié l’impact de l’obésité associée ou non à l’activité physique sur la croissance tumorale et sur le statut oxydatif et inflammatoire des tumeurs à l’aide d’un modèle de souris âgées C57BL/6 nourries avec un régime hyper-lipidique (HL) pendant 14 semaines, et hébergées soit dans un environnement enrichi (EE) pour favoriser l’activité physique et les interactions sociales, soit dans un environnement standard pendant 8 semaines, après quoi des cellules syngéniques de tumeur mammaire EO771 ont été implantées dans les quatrièmes coussinets adipeux mammaires. In vitro, la leptine a stimulé la production de ROS de façon indépendante de la dose et cette augmentation était dépendante de la production d'O2 cytosolique. Les résultats montrent une augmentation significative du poids dans les groupes recevant le régime HL à prise alimentaire journalière identique. La composition… Advisors/Committee Members: Vasson, Marie-Paule (thesis director).

Subjects/Keywords: Cancer du sein; Leptine; Obésité; Leptin; Mammary epithelial cells; Obesity; Oxidative status; Carcinogenesis; 610

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APA (6^th Edition):

Mahbouli, S. (2015). Etude de l'impact de la leptine sur le statut oxydatif et inflammatoire du tissu mammaire : approche expérimentale in vitro et in vivo - Mise en oeuvre de la technique de détection par fluorescence native. : Impact of leptin on oxidative and inflammatory status of the mammary tissue. An in-vitro and in- vivo experimental approach using the native fluorescence detection technique. (Doctoral Dissertation). Clermont-Ferrand 1. Retrieved from http://www.theses.fr/2015CLF1PP04

Chicago Manual of Style (16^th Edition):

Mahbouli, Sinda. “Etude de l'impact de la leptine sur le statut oxydatif et inflammatoire du tissu mammaire : approche expérimentale in vitro et in vivo - Mise en oeuvre de la technique de détection par fluorescence native. : Impact of leptin on oxidative and inflammatory status of the mammary tissue. An in-vitro and in- vivo experimental approach using the native fluorescence detection technique.” 2015. Doctoral Dissertation, Clermont-Ferrand 1. Accessed March 03, 2021. http://www.theses.fr/2015CLF1PP04.

MLA Handbook (7^th Edition):

Mahbouli, Sinda. “Etude de l'impact de la leptine sur le statut oxydatif et inflammatoire du tissu mammaire : approche expérimentale in vitro et in vivo - Mise en oeuvre de la technique de détection par fluorescence native. : Impact of leptin on oxidative and inflammatory status of the mammary tissue. An in-vitro and in- vivo experimental approach using the native fluorescence detection technique.” 2015. Web. 03 Mar 2021.

Vancouver:

Mahbouli S. Etude de l'impact de la leptine sur le statut oxydatif et inflammatoire du tissu mammaire : approche expérimentale in vitro et in vivo - Mise en oeuvre de la technique de détection par fluorescence native. : Impact of leptin on oxidative and inflammatory status of the mammary tissue. An in-vitro and in- vivo experimental approach using the native fluorescence detection technique. [Internet] [Doctoral dissertation]. Clermont-Ferrand 1; 2015. [cited 2021 Mar 03]. Available from: http://www.theses.fr/2015CLF1PP04.

Council of Science Editors:

Mahbouli S. Etude de l'impact de la leptine sur le statut oxydatif et inflammatoire du tissu mammaire : approche expérimentale in vitro et in vivo - Mise en oeuvre de la technique de détection par fluorescence native. : Impact of leptin on oxidative and inflammatory status of the mammary tissue. An in-vitro and in- vivo experimental approach using the native fluorescence detection technique. [Doctoral Dissertation]. Clermont-Ferrand 1; 2015. Available from: http://www.theses.fr/2015CLF1PP04

12. Moreno Layseca, Paulina. The role of β1-integrin in normal and oncogene-mediated proliferation in breast epithelia.

Degree: 2015, University of Manchester

URL: http://www.manchester.ac.uk/escholar/uk-ac-man-scw:257069

► Luminal epithelial cells in the mammary gland require two types of signals to proliferate: soluble signals (growth factor signals) and signals from the extracellular matrix… (more)

▼ Luminal epithelial cells in the mammary gland require two types of signals to proliferate: soluble signals (growth factor signals) and signals from the extracellular matrix (ECM). The composition of the ECM is sensed by adhesion receptors such as integrins. Integrins modulate cell behaviour and play a key role in cell cycle entry. Altered integrin expression and signalling has been associated with breast cancer and studies using mouse mammary epithelial cells (MECs) have shown that the absence of β1-integrin induces growth arrest. However, it is not completely understood how integrins transduce the signals from the plasma membrane to the nucleus to induce cell cycle entry. Thus, the first aim of this project was to determine how β1-integrin controls proliferation in MECs. I established a model to study the effects of depleting β1-integrin using the FSK7 mammary epithelial cell line. The proliferation defect observed in this β1-integrin knockdown model was rescued by expressing a constitutively active Rac1 or Pak. Moreover, inhibiting Rac1 or Pak prevented normal proliferation in MECs in a similar fashion as β1-integrin depletion. Furthermore, in this thesis I have identified the complex comprised of Src, paxillin and p130Cas as a potential link between β1-integrin and Rac1. These results provide an insight into the mechanism that regulates proliferation downstream of β1-integrin. During breast cancer initiation, β1-integrin signals are disrupted. This indicates that additional signals must be driving proliferation during tumorigenesis. Therefore, the second aim of this project was to test whether expression of breast oncogenes can overcome the proliferation defect present in β1-integrin null cells. In order to do so, an oncogenic ErbB2, a constitutively active form of Akt (myrAkt) and the Notch1 intracellular domain (NICD) were transfected in the β1-integrin knockdown MECs. The results showed that ErbB2 overcomes the need for β1-integrin by signalling to Pak. NICD does not require β1-integrin to drive proliferation by an unknown mechanism. Expression of myrAkt did not restore normal levels of proliferation in β1-integrin depleted MECs. This finding suggests that Akt is not sufficient to induce cell cycle entry by itself and instead, both Akt and Erk signalling are needed to exert this function. This work has further delineated the specific signals controlling proliferation downstream of β1-integrin, and has provided a model to test the dependence of oncogenes for β1-integrin to drive proliferation in MECs. These studies are important to understand the role of β1-integrin in breast cancer formation and to define the types of breast cancer where β1-integrin can be used as an effective therapeutic target. Advisors/Committee Members: WELLBROCK, CLAUDIA C, Streuli, Charles, Wellbrock, Claudia.

Subjects/Keywords: Integrins; Proliferation; Mammary epithelial cells

…impact of adhesion receptors on mammary epithelial cells proliferation… …Mammary epithelial cells Myosin-light chain kinase Modulator of Non-genomic Action of estrogen… …associated with breast cancer and studies using mouse mammary epithelial cells (MECs)… …The epithelial cells forming the mammary gland ducts require adhesion to the extracellular… …low levels of p27 or p21 in neurons and mammary epithelial cells, respectively (Blaess…

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APA (6^th Edition):

Moreno Layseca, P. (2015). The role of β1-integrin in normal and oncogene-mediated proliferation in breast epithelia. (Doctoral Dissertation). University of Manchester. Retrieved from http://www.manchester.ac.uk/escholar/uk-ac-man-scw:257069

Chicago Manual of Style (16^th Edition):

Moreno Layseca, Paulina. “The role of β1-integrin in normal and oncogene-mediated proliferation in breast epithelia.” 2015. Doctoral Dissertation, University of Manchester. Accessed March 03, 2021. http://www.manchester.ac.uk/escholar/uk-ac-man-scw:257069.

MLA Handbook (7^th Edition):

Moreno Layseca, Paulina. “The role of β1-integrin in normal and oncogene-mediated proliferation in breast epithelia.” 2015. Web. 03 Mar 2021.

Vancouver:

Moreno Layseca P. The role of β1-integrin in normal and oncogene-mediated proliferation in breast epithelia. [Internet] [Doctoral dissertation]. University of Manchester; 2015. [cited 2021 Mar 03]. Available from: http://www.manchester.ac.uk/escholar/uk-ac-man-scw:257069.

Council of Science Editors:

Moreno Layseca P. The role of β1-integrin in normal and oncogene-mediated proliferation in breast epithelia. [Doctoral Dissertation]. University of Manchester; 2015. Available from: http://www.manchester.ac.uk/escholar/uk-ac-man-scw:257069

University of Colorado

13. Han, Yu. Remodeling of Zinc Homeostasis in Differentiated Mammary Epithelial Cells.

Degree: PhD, 2018, University of Colorado

URL: https://scholar.colorado.edu/chem_gradetds/287

► Zinc is the second most abundant transition metal in mammals and an essential nutrient required for growth. Coupled with the biological significance of zinc, zinc… (more)

Subjects/Keywords: zinc homeostasis; mammary epithelial cells; biological functions; milk protein; remodeling; Biochemistry; Physiology

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APA (6^th Edition):

Han, Y. (2018). Remodeling of Zinc Homeostasis in Differentiated Mammary Epithelial Cells. (Doctoral Dissertation). University of Colorado. Retrieved from https://scholar.colorado.edu/chem_gradetds/287

Chicago Manual of Style (16^th Edition):

Han, Yu. “Remodeling of Zinc Homeostasis in Differentiated Mammary Epithelial Cells.” 2018. Doctoral Dissertation, University of Colorado. Accessed March 03, 2021. https://scholar.colorado.edu/chem_gradetds/287.

MLA Handbook (7^th Edition):

Han, Yu. “Remodeling of Zinc Homeostasis in Differentiated Mammary Epithelial Cells.” 2018. Web. 03 Mar 2021.

Vancouver:

Han Y. Remodeling of Zinc Homeostasis in Differentiated Mammary Epithelial Cells. [Internet] [Doctoral dissertation]. University of Colorado; 2018. [cited 2021 Mar 03]. Available from: https://scholar.colorado.edu/chem_gradetds/287.

Council of Science Editors:

Han Y. Remodeling of Zinc Homeostasis in Differentiated Mammary Epithelial Cells. [Doctoral Dissertation]. University of Colorado; 2018. Available from: https://scholar.colorado.edu/chem_gradetds/287

Queen Mary, University of London

14. Braker, Paul. ABCB5 and the regulation of p16INK4a by non-coding RNA.

Degree: PhD, 2014, Queen Mary, University of London

URL: http://qmro.qmul.ac.uk/xmlui/handle/123456789/7930 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.658673

► p16INK4a (p16) traps the cell at the restriction point of the cell cycle by binding to cyclin-dependent kinase 4/6 thus preventing the phosphorylation of the… (more)

▼ p16INK4a (p16) traps the cell at the restriction point of the cell cycle by binding to cyclin-dependent kinase 4/6 thus preventing the phosphorylation of the retinoblastoma protein (pRB). As p16 accumulates the cell stops dividing and becomes senescent. This study investigates the modulation of p16 function by the putative membrane protein ABCB5 and a group of five putative oncogenic microRNAs (oncomiRs). ABCB5 is a poorly characterised member of the B-subfamily of human ATP Binding Cassette transporters. ABCB5 is reportedly transcribed into four transcripts, one of which could potentially encode a full-length transporter (ABCB5fl) whilst a second could encode a half-transporter (ABCB5β). The other two transcripts (ABCB5α and ABCB5γ) could only encode short polypeptides. Exogenous expression of ABCB5fl and ABCB5β was achieved in HEK293T cells, but the recombinant protein expressed poorly and localised to the endoplasmic reticulum. Point mutations introduced into the ATP catalytic domain failed to improve expression levels suggesting that protein function was not deleterious to the cell. Exogenous expression in HEK293T cells also allowed commercial antibodies purportedly raised against ABCB5 isoforms to be tested. Several were found not to recognise ABCB5 necessitating re-interpretation of published data. However, one antibody recognised both ABCB5fl and ABCB5β, and was subsequently used to evaluate protein expression levels in other cell types.siRNA knockdown of ABCB5 in human mammary epithelial cells (HMECs) caused a concomitant reduction in p16 expression and an increase in cellular proliferation. Differential siRNAs and RT-qPCR analyses demonstrated ABCB5β to be the relevant transcript with respect to the reduction in p16 expression; however, no native ABCB5β protein was detected in HMECs. Together these data lead to the hypothesis that the ABCB5β transcript may act as a long noncoding RNA to regulate p16. Exogenous expression of each of five distinct putative oncomiRs in HMECs was found to increase cellular proliferation and, surprisingly, increase p16 expression. These results mirror a phenotype commonly observed in p16-positive basal-like breast cancer (BLBC), an aggressive form of breast cancer with poor prognosis and few treatment options. Bioinformatic analysis of the predicted target genes for these oncomiRs identified multiple transcriptional regulators of pRB. These predictions, together with the work performed in a cellular model of p16-positive BLBC, suggest that the oncomiRs may cause unrestricted cell proliferation by indirectly reducing transcription of the pRB gene, RB1. In the absence of pRB, p16 expression is induced via a previously reported oncogeneinduced senescence-like positive feedback loop. These data, and previously published observations, suggest that a similar mechanism may explain the basis of p16-positive BLBC.

Subjects/Keywords: 572.8; ncogenic microRNAs; cell cycles; tumour suppressor genes; Human Mammary Epithelial Cells.

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APA (6^th Edition):

Braker, P. (2014). ABCB5 and the regulation of p16INK4a by non-coding RNA. (Doctoral Dissertation). Queen Mary, University of London. Retrieved from http://qmro.qmul.ac.uk/xmlui/handle/123456789/7930 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.658673

Chicago Manual of Style (16^th Edition):

Braker, Paul. “ABCB5 and the regulation of p16INK4a by non-coding RNA.” 2014. Doctoral Dissertation, Queen Mary, University of London. Accessed March 03, 2021. http://qmro.qmul.ac.uk/xmlui/handle/123456789/7930 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.658673.

MLA Handbook (7^th Edition):

Braker, Paul. “ABCB5 and the regulation of p16INK4a by non-coding RNA.” 2014. Web. 03 Mar 2021.

Vancouver:

Braker P. ABCB5 and the regulation of p16INK4a by non-coding RNA. [Internet] [Doctoral dissertation]. Queen Mary, University of London; 2014. [cited 2021 Mar 03]. Available from: http://qmro.qmul.ac.uk/xmlui/handle/123456789/7930 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.658673.

Council of Science Editors:

Braker P. ABCB5 and the regulation of p16INK4a by non-coding RNA. [Doctoral Dissertation]. Queen Mary, University of London; 2014. Available from: http://qmro.qmul.ac.uk/xmlui/handle/123456789/7930 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.658673

University of Texas – Austin

15. Smith, Gail Perry. Mouse mammary tumor virus activates Cdc42 leading to filopodia formation and transformation of mammary epithelial cells.

Degree: PhD, Ecology, Evolution and Behavior ; Microbiology ; Plant Biology, 2005, University of Texas – Austin

URL: http://hdl.handle.net/2152/1731

► Mouse mammary tumor virus (MMTV) is a B type retrovirus characterized by assembly of viral “A” particles in the cytoplasm that move to the membrane… (more)

Subjects/Keywords: Mouse mammary tumor virus; Epithelial cells

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APA (6^th Edition):

Smith, G. P. (2005). Mouse mammary tumor virus activates Cdc42 leading to filopodia formation and transformation of mammary epithelial cells. (Doctoral Dissertation). University of Texas – Austin. Retrieved from http://hdl.handle.net/2152/1731

Chicago Manual of Style (16^th Edition):

Smith, Gail Perry. “Mouse mammary tumor virus activates Cdc42 leading to filopodia formation and transformation of mammary epithelial cells.” 2005. Doctoral Dissertation, University of Texas – Austin. Accessed March 03, 2021. http://hdl.handle.net/2152/1731.

MLA Handbook (7^th Edition):

Smith, Gail Perry. “Mouse mammary tumor virus activates Cdc42 leading to filopodia formation and transformation of mammary epithelial cells.” 2005. Web. 03 Mar 2021.

Vancouver:

Smith GP. Mouse mammary tumor virus activates Cdc42 leading to filopodia formation and transformation of mammary epithelial cells. [Internet] [Doctoral dissertation]. University of Texas – Austin; 2005. [cited 2021 Mar 03]. Available from: http://hdl.handle.net/2152/1731.

Council of Science Editors:

Smith GP. Mouse mammary tumor virus activates Cdc42 leading to filopodia formation and transformation of mammary epithelial cells. [Doctoral Dissertation]. University of Texas – Austin; 2005. Available from: http://hdl.handle.net/2152/1731

Utah State University

16. Kurz, Jacqueline P. Bovine Mastitis Resistance: Novel Quantitative Trait Loci and the Role of Bovine Mammary Epithelial Cells.

Degree: PhD, Animal, Dairy, and Veterinary Sciences, 2018, Utah State University

URL: https://digitalcommons.usu.edu/etd/6910

► Bovine mastitis, or inflammation of the mammary gland, has substantial economic and animal welfare implications. A genetic basis for mastitis resistance traits is recognized… (more)

Subjects/Keywords: bovine mastitis; GWAS; QTL; bovine mammary epithelial cells; Animal Sciences; Dairy Science; Veterinary Medicine

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APA (6^th Edition):

Kurz, J. P. (2018). Bovine Mastitis Resistance: Novel Quantitative Trait Loci and the Role of Bovine Mammary Epithelial Cells. (Doctoral Dissertation). Utah State University. Retrieved from https://digitalcommons.usu.edu/etd/6910

Chicago Manual of Style (16^th Edition):

Kurz, Jacqueline P. “Bovine Mastitis Resistance: Novel Quantitative Trait Loci and the Role of Bovine Mammary Epithelial Cells.” 2018. Doctoral Dissertation, Utah State University. Accessed March 03, 2021. https://digitalcommons.usu.edu/etd/6910.

MLA Handbook (7^th Edition):

Kurz, Jacqueline P. “Bovine Mastitis Resistance: Novel Quantitative Trait Loci and the Role of Bovine Mammary Epithelial Cells.” 2018. Web. 03 Mar 2021.

Vancouver:

Kurz JP. Bovine Mastitis Resistance: Novel Quantitative Trait Loci and the Role of Bovine Mammary Epithelial Cells. [Internet] [Doctoral dissertation]. Utah State University; 2018. [cited 2021 Mar 03]. Available from: https://digitalcommons.usu.edu/etd/6910.

Council of Science Editors:

Kurz JP. Bovine Mastitis Resistance: Novel Quantitative Trait Loci and the Role of Bovine Mammary Epithelial Cells. [Doctoral Dissertation]. Utah State University; 2018. Available from: https://digitalcommons.usu.edu/etd/6910

17. Abi Khalil, Amanda. Modulation du phénotype dans les cellules HMEC : Phenotype modulation in HMEc.

Degree: Docteur es, Biologie Santé, 2017, Montpellier

URL: http://www.theses.fr/2017MONTT013

►

Le cancer du sein est une pathologie hétérogène au plan clinique et au moins 5 sous-types moléculaires ont pu être définis sur la base de… (more)

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Le cancer du sein est une pathologie hétérogène au plan clinique et au moins 5 sous-types moléculaires ont pu être définis sur la base de différences d’expression ARNm. Ces sous-types présentent des différences de profils d’anomalies génomiques et de méthylation des cytosines. Ces différences génétiques et épigénétiques s’expliqueraient par des types cellulaires d’origines distincts au sein de l’épithélium mammaire, toutefois, ceci n’a pas été confirmé clairement à ce jour. Alternativement, il a été proposé que l’activation de voies oncogéniques différentes pouvait avoir un impact significatif sur les modifications génétiques ou épigénétiques. Dans ce travail nous avons voulu vérifier cette hypothèse en l’appliquant à un modèle de cellules épithéliales mammaires normales primaires humaines, que nous avons isolé des à partir de glandes mammaires. Ces cellules ont été transformées en deux étapes par transduction avec (i) un shARN ciblant TP53, (ii) un oncogène. Nous avons sélectionné 3 oncogènes qui activent des voies de signalisations distinctes CCNE1, HRAS-v12 et WNT1. Nous avons établi un modèle de transformation tumorale en trois étapes, cellules normales, immortalisées et transformées, permettant de suivre les modifications moléculaires associées à chaque étape et de vérifier si l’activation de voies oncogéniques distinctes produisait des profils d’anomalies différents. Les différents modèles ont été analysés par CGH-array, RRBS, transcriptome et miRNA à des temps de culture définis.Nos résultats montrent que l’activation de la voie RAS aboutit à des profils d’anomalies génétiques et de méthylation des CpG radicalement différents de ceux obtenus après surexpression des gènes CCNE1 et WNT1. Ces différences apparaissent très rapidement après transduction des oncogènes alors que les profils des cellules CCNE1 et WNT1 divergent plus tardivement. Enfin, l’inactivation de p53 n’induit pas par elle-même une instabilité élevée, mais produit un contexte de plasticité favorable aux modifications génétiques et épigénétique.Par ailleurs, nous avons noté des différences phénotypiques entre les HMEC RAS (mésenchymateuses) et les HMEC CCNE1 et les HMEC WNT1 (épithéliales). Dans ce travail, je montre que les HMEC shp53 immortalisées présentent une plasticité phénotypique, une partie des cellules entrant en EMT spontanément, l’autre restant épithéliales. J’ai montré que la transduction RAS sélectionnait les cellules ayant effectué une EMT, alors que la transduction de CCNE1 ou WNT1 sélectionnait les cellules épithéliales. J’ai cherché à identifier les déterminants de ces changements phénotypiques et mes résultats suggèrent qu’ils résultent d’une balance entre une signalisation TGFB1/BMP1, qui favorise l’EMT, et BMP4/WNT7 qui favorise la MET.

Breast cancer is a heterogeneous pathology. Based on the differences of mRNA expression, at least five molecular subtypes have been defined. These subtypes show differences in profiles of genomic abnormalities and CpG methylation. These molecular subtypes are thought to originate from…

Advisors/Committee Members: Theillet, Charles (thesis director).

Subjects/Keywords: Phénotype; Cellules épitheliales mammaires primaires; Transition épithélio-Mésenchymateuse; Phenotype; Human mammary epithelial cells; Epithelial-Mesenchymal transition

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APA (6^th Edition):

Abi Khalil, A. (2017). Modulation du phénotype dans les cellules HMEC : Phenotype modulation in HMEc. (Doctoral Dissertation). Montpellier. Retrieved from http://www.theses.fr/2017MONTT013

Chicago Manual of Style (16^th Edition):

Abi Khalil, Amanda. “Modulation du phénotype dans les cellules HMEC : Phenotype modulation in HMEc.” 2017. Doctoral Dissertation, Montpellier. Accessed March 03, 2021. http://www.theses.fr/2017MONTT013.

MLA Handbook (7^th Edition):

Abi Khalil, Amanda. “Modulation du phénotype dans les cellules HMEC : Phenotype modulation in HMEc.” 2017. Web. 03 Mar 2021.

Vancouver:

Abi Khalil A. Modulation du phénotype dans les cellules HMEC : Phenotype modulation in HMEc. [Internet] [Doctoral dissertation]. Montpellier; 2017. [cited 2021 Mar 03]. Available from: http://www.theses.fr/2017MONTT013.

Council of Science Editors:

Abi Khalil A. Modulation du phénotype dans les cellules HMEC : Phenotype modulation in HMEc. [Doctoral Dissertation]. Montpellier; 2017. Available from: http://www.theses.fr/2017MONTT013

18. FAN YIPING. The Search for Stem Cell in Human Breast Milk.

Degree: 2010, National University of Singapore

URL: http://scholarbank.nus.edu.sg/handle/10635/20970

Subjects/Keywords: Mammary Stem Cells; Breast Milk; Epithelial; Haemopoietic Stem Cells

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APA (6^th Edition):

YIPING, F. (2010). The Search for Stem Cell in Human Breast Milk. (Thesis). National University of Singapore. Retrieved from http://scholarbank.nus.edu.sg/handle/10635/20970

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):

YIPING, FAN. “The Search for Stem Cell in Human Breast Milk.” 2010. Thesis, National University of Singapore. Accessed March 03, 2021. http://scholarbank.nus.edu.sg/handle/10635/20970.

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

MLA Handbook (7^th Edition):

YIPING, FAN. “The Search for Stem Cell in Human Breast Milk.” 2010. Web. 03 Mar 2021.

Vancouver:

YIPING F. The Search for Stem Cell in Human Breast Milk. [Internet] [Thesis]. National University of Singapore; 2010. [cited 2021 Mar 03]. Available from: http://scholarbank.nus.edu.sg/handle/10635/20970.

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

Council of Science Editors:

YIPING F. The Search for Stem Cell in Human Breast Milk. [Thesis]. National University of Singapore; 2010. Available from: http://scholarbank.nus.edu.sg/handle/10635/20970

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

University of Cambridge

19. Harris, Olivia. Elucidation of mammary gland development: combination of novel techniques to study proliferation and stem cells.

Degree: PhD, 2019, University of Cambridge

URL: https://www.repository.cam.ac.uk/handle/1810/291054

► The mammary gland is a dynamic organ that undergoes many cycles of proliferation and death throughout both oestrus cycling and the gestation/lactation/involution cycle. Moreover, it… (more)

▼ The mammary gland is a dynamic organ that undergoes many cycles of proliferation and death throughout both oestrus cycling and the gestation/lactation/involution cycle. Moreover, it is a unique tissue in that the majority of its development occurs postnatally coincident with the production of ovarian hormones in puberty. This capacity of the mammary gland for rapid growth and regeneration has been attributed to mammary stem cells (MaSCs). However, despite extensive efforts over the past 60 years, definitive characterisation of the stem and progenitor cells of the mammary gland has yet to be achieved. A number of recent conflicting, lineage tracing studies have served only to fuel the fires of controversy, with previous characterisation of the mammary gland largely carried out using two-dimensional tissue sections. However, in order to fully appreciate the capacity of MaSCs and to maintain spatial information of the complex topological structure, the mammary gland must be investigated in its intact form. Accordingly, there is still much disagreement regarding the potency, capacity and location of MaSCs. Consequently, in order to unequivocally elucidate the MaSC hierarchy, a variety of novel techniques have been combined in this thesis. The first involves development and optimisation of optical tissue clearing techniques to allow the visualisation of the native mammary gland, in situ, and in three dimensions. To do so, a number of different optical tissue clearing methods have been assessed and combined with a variety of microscopy techniques to allow the multiple focal planes of the ductal network to be examined. These imaging techniques were then combined with two neutral lineage tracing models; the first, the Rosa26[CA]30 model, utilises stochastic continuous clonal labelling to allow for the fate tracking of the progeny from single functional stem and progenitor cells. The second unbiased lineage tracing approach, the Rosa26-Confetti model, allows for the mammary stem and progenitor progeny to be traced with precise timing, with the additional benefit of a multicolour reporter. Next, proliferation was examined in wholemount tissues to investigate the functional requirements for MaSCs, and their potential locations. Finally, these techniques have been combined with an ex vivo 3D organoid culture system to investigate the use of culture methods in examining mammary epithelial cell dynamics. By combination of these techniques, clonally marked regions can be investigated throughout the development of the mammary gland, from the formation of the embryonic mammary iii rudiment, to expansion of the ductal tree in puberty, and ultimately their fate in lactation and involution, where the mammary gland fulfils its evolutionary purpose. The mammary gland provides a unique opportunity to investigate epithelial development extra-embryonically that is not available in other tissues. Moreover, study of maintenance and turnover of this organ has important implications for other epithelial systems. Finally, elucidation of the…

Subjects/Keywords: stem cells; mammary gland; adult stem cells; lineage tracing; proliferation; breast; breast cancer; MaSC; MaSCs; mammary gland stem cells; mammary stem cells; confetti; CA30; organoids; 3D models; mammary gland organoids; epithelial biology; epithelial organoids; ex vivo culture; optical clearing; optical tissue clearing; CUBIC; SeeDB; 3DISCO; confocal; 3D imaging; advanced microscopy; advanced imaging; 3D confocal

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

APA (6^th Edition):

Harris, O. (2019). Elucidation of mammary gland development: combination of novel techniques to study proliferation and stem cells. (Doctoral Dissertation). University of Cambridge. Retrieved from https://www.repository.cam.ac.uk/handle/1810/291054

Chicago Manual of Style (16^th Edition):

Harris, Olivia. “Elucidation of mammary gland development: combination of novel techniques to study proliferation and stem cells.” 2019. Doctoral Dissertation, University of Cambridge. Accessed March 03, 2021. https://www.repository.cam.ac.uk/handle/1810/291054.

MLA Handbook (7^th Edition):

Harris, Olivia. “Elucidation of mammary gland development: combination of novel techniques to study proliferation and stem cells.” 2019. Web. 03 Mar 2021.

Vancouver:

Harris O. Elucidation of mammary gland development: combination of novel techniques to study proliferation and stem cells. [Internet] [Doctoral dissertation]. University of Cambridge; 2019. [cited 2021 Mar 03]. Available from: https://www.repository.cam.ac.uk/handle/1810/291054.

Council of Science Editors:

Harris O. Elucidation of mammary gland development: combination of novel techniques to study proliferation and stem cells. [Doctoral Dissertation]. University of Cambridge; 2019. Available from: https://www.repository.cam.ac.uk/handle/1810/291054

University of Cambridge

20. Harris, Olivia. Elucidation of mammary gland development : combination of novel techniques to study proliferation and stem cells.

Degree: PhD, 2019, University of Cambridge

URL: https://doi.org/10.17863/CAM.38235 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.774673

► The mammary gland is a dynamic organ that undergoes many cycles of proliferation and death throughout both oestrus cycling and the gestation/lactation/involution cycle. Moreover, it… (more)

▼ The mammary gland is a dynamic organ that undergoes many cycles of proliferation and death throughout both oestrus cycling and the gestation/lactation/involution cycle. Moreover, it is a unique tissue in that the majority of its development occurs postnatally coincident with the production of ovarian hormones in puberty. This capacity of the mammary gland for rapid growth and regeneration has been attributed to mammary stem cells (MaSCs). However, despite extensive efforts over the past 60 years, definitive characterisation of the stem and progenitor cells of the mammary gland has yet to be achieved. A number of recent conflicting, lineage tracing studies have served only to fuel the fires of controversy, with previous characterisation of the mammary gland largely carried out using two-dimensional tissue sections. However, in order to fully appreciate the capacity of MaSCs and to maintain spatial information of the complex topological structure, the mammary gland must be investigated in its intact form. Accordingly, there is still much disagreement regarding the potency, capacity and location of MaSCs. Consequently, in order to unequivocally elucidate the MaSC hierarchy, a variety of novel techniques have been combined in this thesis. The first involves development and optimisation of optical tissue clearing techniques to allow the visualisation of the native mammary gland, in situ, and in three dimensions. To do so, a number of different optical tissue clearing methods have been assessed and combined with a variety of microscopy techniques to allow the multiple focal planes of the ductal network to be examined. These imaging techniques were then combined with two neutral lineage tracing models; the first, the Rosa26[CA]30 model, utilises stochastic continuous clonal labelling to allow for the fate tracking of the progeny from single functional stem and progenitor cells. The second unbiased lineage tracing approach, the Rosa26-Confetti model, allows for the mammary stem and progenitor progeny to be traced with precise timing, with the additional benefit of a multicolour reporter. Next, proliferation was examined in wholemount tissues to investigate the functional requirements for MaSCs, and their potential locations. Finally, these techniques have been combined with an ex vivo 3D organoid culture system to investigate the use of culture methods in examining mammary epithelial cell dynamics. By combination of these techniques, clonally marked regions can be investigated throughout the development of the mammary gland, from the formation of the embryonic mammary iii rudiment, to expansion of the ductal tree in puberty, and ultimately their fate in lactation and involution, where the mammary gland fulfils its evolutionary purpose. The mammary gland provides a unique opportunity to investigate epithelial development extra-embryonically that is not available in other tissues. Moreover, study of maintenance and turnover of this organ has important implications for other epithelial systems. Finally, elucidation of the…

Subjects/Keywords: stem cells; mammary gland; adult stem cells; lineage tracing; proliferation; breast; breast cancer; MaSC; MaSCs; mammary gland stem cells; mammary stem cells; confetti; CA30; organoids; 3D models; mammary gland organoids; epithelial biology; epithelial organoids; ex vivo culture; optical clearing; optical tissue clearing; CUBIC; SeeDB; 3DISCO; confocal; 3D imaging; advanced microscopy; advanced imaging; 3D confocal

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❌

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

APA (6^th Edition):

Harris, O. (2019). Elucidation of mammary gland development : combination of novel techniques to study proliferation and stem cells. (Doctoral Dissertation). University of Cambridge. Retrieved from https://doi.org/10.17863/CAM.38235 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.774673

Chicago Manual of Style (16^th Edition):

Harris, Olivia. “Elucidation of mammary gland development : combination of novel techniques to study proliferation and stem cells.” 2019. Doctoral Dissertation, University of Cambridge. Accessed March 03, 2021. https://doi.org/10.17863/CAM.38235 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.774673.

MLA Handbook (7^th Edition):

Harris, Olivia. “Elucidation of mammary gland development : combination of novel techniques to study proliferation and stem cells.” 2019. Web. 03 Mar 2021.

Vancouver:

Harris O. Elucidation of mammary gland development : combination of novel techniques to study proliferation and stem cells. [Internet] [Doctoral dissertation]. University of Cambridge; 2019. [cited 2021 Mar 03]. Available from: https://doi.org/10.17863/CAM.38235 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.774673.

Council of Science Editors:

Harris O. Elucidation of mammary gland development : combination of novel techniques to study proliferation and stem cells. [Doctoral Dissertation]. University of Cambridge; 2019. Available from: https://doi.org/10.17863/CAM.38235 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.774673

21. Chang, Cheng. Function and Regulation of the α6 Integrins in Mammary Epithelial Biology and Breast Cancer: A Dissertation.

Degree: Cancer Biology, Molecular, Cell and Cancer Biology Department, 2015, U of Massachusetts : Med

URL: http://escholarship.umassmed.edu/gsbs_diss/734

► Integrins have the ability to impact major aspects of epithelial biology including adhesion, migration, invasion, signaling and differentiation, as well as the formation and… (more)

▼ Integrins have the ability to impact major aspects of epithelial biology including adhesion, migration, invasion, signaling and differentiation, as well as the formation and progression of cancer (Hynes 2002; Srichai and Zent 2010; Anderson et al. 2014). This thesis focuses on how integrins are regulated and function in the context of mammary epithelial biology and breast cancer with a specific focus on the α6 integrin heterodimers (α6β1 and α6β4). These integrins function primarily as receptors for the laminin family of extracellular matrix (ECM) proteins and they have been implicated in mammary gland biology and breast cancer (Friedrichs et al. 1995; Wewer et al. 1997; Mercurio et al. 2001; Margadant and Sonnenberg 2010; Muschler and Streuli 2010; Nistico et al. 2014). The first project investigates how alternative splicing of the α6 subunit impacts the genesis and function of breast cancer stem cells (CSCs). This work revealed that the α6Bβ1 splice variant, but not α6Aβ1, is necessary for the function of breast CSCs because it activates the Hippo transducer TAZ (Zhao et al. 2008a), which is known to be essential for breast CSCs (Cordenonsi et al. 2011). My work also led to the discovery that laminin (LM) 511 is the specific ligand for α6Bβ1 and that autocrine LM511, which is mediated by TAZ, is needed to sustain breast CSCs by functioning as a ‘ECM niche’. An important aspect of this study is the finding that surface-bound LM511 characterizes a small population of cells in human breast tumors with CSC properties. The second project of my thesis concentrated on identifying transcription factors that regulate expression of the β4 subunit. The expression of the α6β4 integrin is repressed during the epithelial-mesenchymal transition (EMT) (Yang et al. 2009) but the contribution of specific transcription factors to this repression is poorly understood. This study revealed that Snai1 is a transcriptional repressor of β4, which is responsible for establishing the PRC2 (Polycomb complex 2)- associated repressive histone mark H3K27Me3. However, I also found that the ability of Snai1 to repress transcription is abrogated by its interaction with Id2. Specifically, I identified the biochemical mechanism for how Id2 regulates Snai1. Id2 binds the SNAG domain of Snai1 that is the docking site for several corepressors (Peinado et al. 2004; Lin et al. 2010b; Dong et al. 2012a). One important consequence of Id2 interacting with Snai1 on the β4 promoter is that it prevents repressive epigenetic modifications. This finding may explain why some epithelial cells express Snai1 and β4 because they also express Id2 (Vincent et al. 2009; Bastea et al. 2012). The repression of the α6β4 integrin during the EMT is consistent with data indicating that this integrin is not expressed in CSCs (Mani et al. 2008; Goel et al. 2012; Goel et al. 2013; Goel et al. 2014). An important question going forward is to understand how the α6β4 integrin contributes to tumor formation. In summary, my thesis provides novel insights into… Advisors/Committee Members: Arthur Mercurio, PhD.

Subjects/Keywords: Integrin alpha6; Breast Neoplasms; Epithelial Cells; Human Mammary Glands; Cancer Biology; Cell Biology; Cellular and Molecular Physiology; Neoplasms

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APA (6^th Edition):

Chang, C. (2015). Function and Regulation of the α6 Integrins in Mammary Epithelial Biology and Breast Cancer: A Dissertation. (Doctoral Dissertation). U of Massachusetts : Med. Retrieved from http://escholarship.umassmed.edu/gsbs_diss/734

Chicago Manual of Style (16^th Edition):

Chang, Cheng. “Function and Regulation of the α6 Integrins in Mammary Epithelial Biology and Breast Cancer: A Dissertation.” 2015. Doctoral Dissertation, U of Massachusetts : Med. Accessed March 03, 2021. http://escholarship.umassmed.edu/gsbs_diss/734.

MLA Handbook (7^th Edition):

Chang, Cheng. “Function and Regulation of the α6 Integrins in Mammary Epithelial Biology and Breast Cancer: A Dissertation.” 2015. Web. 03 Mar 2021.

Vancouver:

Chang C. Function and Regulation of the α6 Integrins in Mammary Epithelial Biology and Breast Cancer: A Dissertation. [Internet] [Doctoral dissertation]. U of Massachusetts : Med; 2015. [cited 2021 Mar 03]. Available from: http://escholarship.umassmed.edu/gsbs_diss/734.

Council of Science Editors:

Chang C. Function and Regulation of the α6 Integrins in Mammary Epithelial Biology and Breast Cancer: A Dissertation. [Doctoral Dissertation]. U of Massachusetts : Med; 2015. Available from: http://escholarship.umassmed.edu/gsbs_diss/734

Vanderbilt University

22. Potdar, Alka Anand. Characterizing eukaryotic single cell motility via bimodal analysis.

Degree: PhD, Chemical Engineering, 2009, Vanderbilt University

URL: http://hdl.handle.net/1803/15284

► Bimodal analysis, a cellular-scale approach to studying eukaryotic single cell migration by performing a model-based analysis of single cell video-microscopy data, is described. The bimodal… (more)

Subjects/Keywords: mammary epithelial cells; video-microscopy; bimodal framework; cell migration

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APA (6^th Edition):

Potdar, A. A. (2009). Characterizing eukaryotic single cell motility via bimodal analysis. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://hdl.handle.net/1803/15284

Chicago Manual of Style (16^th Edition):

Potdar, Alka Anand. “Characterizing eukaryotic single cell motility via bimodal analysis.” 2009. Doctoral Dissertation, Vanderbilt University. Accessed March 03, 2021. http://hdl.handle.net/1803/15284.

MLA Handbook (7^th Edition):

Potdar, Alka Anand. “Characterizing eukaryotic single cell motility via bimodal analysis.” 2009. Web. 03 Mar 2021.

Vancouver:

Potdar AA. Characterizing eukaryotic single cell motility via bimodal analysis. [Internet] [Doctoral dissertation]. Vanderbilt University; 2009. [cited 2021 Mar 03]. Available from: http://hdl.handle.net/1803/15284.

Council of Science Editors:

Potdar AA. Characterizing eukaryotic single cell motility via bimodal analysis. [Doctoral Dissertation]. Vanderbilt University; 2009. Available from: http://hdl.handle.net/1803/15284

Texas Medical Center

23. Caruso, Joseph Anthony. IMBALANCE BETWEEN NEUTROPHIL ELASTASE AND ELAFIN PROMOTES BREAST CANCER GROWTH AND PROGRESSION.

Degree: PhD, 2014, Texas Medical Center

URL: https://digitalcommons.library.tmc.edu/utgsbs_dissertations/433

► Elafin, an endogenous serine protease inhibitor, is a critical component of the epithelial barrier against neutrophil elastase (NE) activity. The central hypothesis examined in… (more)

▼ Elafin, an endogenous serine protease inhibitor, is a critical component of the epithelial barrier against neutrophil elastase (NE) activity. The central hypothesis examined in this dissertation was that elafin has tumor suppressive properties in breast cancer. In support of this hypothesis, immunohistochemical (IHC) analysis revealed that elafin was downregulated in the majority of invasive breast tumors and a subset of pre-invasive ductal carcinoma in situ (DCIS) compared to elafin expression in the normal mammary epithelium. To understand the role of elafin in the mammary epithelium and the impetus for its downregulation during breast tumorigenesis, primary and immortalized human mammary epithelial cells (HMECs) were utilized as a model system. Elafin was highly expressed in G0-arrested HMECs, suggesting a previously unrecognized role for elafin in growth control. Stable knockdown (KD) of elafin compromised the ability of HMECs to maintain G0-arrest during long-term growth factor deprivation. This effect was reversed by re-expression of wild-type elafin but not elafin-M25G lacking protease inhibitory function, suggesting a role for deregulated protease activity. Elafin KD HMECs demonstrated enhanced sensitivity to NE-induced proliferation. Mechanistically, activation of the ERK signaling pathway downstream of toll-like receptor 4 (TLR4) was essential to the mitogenic effect of NE in this system. Compared to HMECs, the majority of breast cancer cell lines lack endogenous elafin expression. Adenoviral-mediated expression of elafin was utilized to evaluate the tumor suppressive properties of elafin in breast cancer cell lines. Rb-status was identified as the critical factor governing the anti-tumor effect of elafin in this system. In breast cancer cell lines expressing functional Rb, the expression of elafin triggered Rb-dependent cell cycle arrest. However, in breast cancer cell lines lacking functional Rb, elafin expression induced caspase-3 dependent apoptotic cell death. Elafin is a critical counterbalance against NE-activity. IHC analysis revealed that high levels of NE-expressing tumor-associated neutrophils (TAN) were associated with reduced recurrence-free survival, high tumor grade, and triple-receptor negative breast cancer (TNBC). ERK-catalyzed phosphorylation of p90RSK (T359/S363) and Rb phosphorylation (S807/811) were significantly enriched in NE-positive breast tumors, suggesting that NE-induced ERK signaling and proliferation may be relevant to human breast cancer. The in vivo role of deregulated NE in breast tumorigenesis was examined in the C3(1)TAg mouse model of TNBC. Knockout of NE in C3(1)TAg mice significantly reduced tumor growth and proliferation. Elafin has tumor suppressive properties in the context of breast cancer and is a critical counterbalance against the growth promoting effect of NE in vitro and in vivo. Deregulated NE-activity is a viable therapeutic target in breast cancer. Advisors/Committee Members: Khandan Keyomarsi, Jeffrey Rosen, Elsa Flores.

Subjects/Keywords: Elafin; Neutrophil Elastase; Breast Cancer; human mammary epithelial cells; serine protease; C3(1)TAg; Cancer Biology; Medicine and Health Sciences

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APA (6^th Edition):

Caruso, J. A. (2014). IMBALANCE BETWEEN NEUTROPHIL ELASTASE AND ELAFIN PROMOTES BREAST CANCER GROWTH AND PROGRESSION. (Doctoral Dissertation). Texas Medical Center. Retrieved from https://digitalcommons.library.tmc.edu/utgsbs_dissertations/433

Chicago Manual of Style (16^th Edition):

Caruso, Joseph Anthony. “IMBALANCE BETWEEN NEUTROPHIL ELASTASE AND ELAFIN PROMOTES BREAST CANCER GROWTH AND PROGRESSION.” 2014. Doctoral Dissertation, Texas Medical Center. Accessed March 03, 2021. https://digitalcommons.library.tmc.edu/utgsbs_dissertations/433.

MLA Handbook (7^th Edition):

Caruso, Joseph Anthony. “IMBALANCE BETWEEN NEUTROPHIL ELASTASE AND ELAFIN PROMOTES BREAST CANCER GROWTH AND PROGRESSION.” 2014. Web. 03 Mar 2021.

Vancouver:

Caruso JA. IMBALANCE BETWEEN NEUTROPHIL ELASTASE AND ELAFIN PROMOTES BREAST CANCER GROWTH AND PROGRESSION. [Internet] [Doctoral dissertation]. Texas Medical Center; 2014. [cited 2021 Mar 03]. Available from: https://digitalcommons.library.tmc.edu/utgsbs_dissertations/433.

Council of Science Editors:

Caruso JA. IMBALANCE BETWEEN NEUTROPHIL ELASTASE AND ELAFIN PROMOTES BREAST CANCER GROWTH AND PROGRESSION. [Doctoral Dissertation]. Texas Medical Center; 2014. Available from: https://digitalcommons.library.tmc.edu/utgsbs_dissertations/433

Michigan State University

24. Etchebarne, Brett Eric. IGF-I and leptin hormonal infusions alter the cell proliferation and transcriptional profile of the prepubertal bovine mammary gland.

Degree: PhD, Department of Animal Science, 2006, Michigan State University

URL: http://etd.lib.msu.edu/islandora/object/etd:34090

Subjects/Keywords: Cattle; Nutrition; Energy metabolism; Mammary glands; Epithelial cells

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APA (6^th Edition):

Etchebarne, B. E. (2006). IGF-I and leptin hormonal infusions alter the cell proliferation and transcriptional profile of the prepubertal bovine mammary gland. (Doctoral Dissertation). Michigan State University. Retrieved from http://etd.lib.msu.edu/islandora/object/etd:34090

Chicago Manual of Style (16^th Edition):

Etchebarne, Brett Eric. “IGF-I and leptin hormonal infusions alter the cell proliferation and transcriptional profile of the prepubertal bovine mammary gland.” 2006. Doctoral Dissertation, Michigan State University. Accessed March 03, 2021. http://etd.lib.msu.edu/islandora/object/etd:34090.

MLA Handbook (7^th Edition):

Etchebarne, Brett Eric. “IGF-I and leptin hormonal infusions alter the cell proliferation and transcriptional profile of the prepubertal bovine mammary gland.” 2006. Web. 03 Mar 2021.

Vancouver:

Etchebarne BE. IGF-I and leptin hormonal infusions alter the cell proliferation and transcriptional profile of the prepubertal bovine mammary gland. [Internet] [Doctoral dissertation]. Michigan State University; 2006. [cited 2021 Mar 03]. Available from: http://etd.lib.msu.edu/islandora/object/etd:34090.

Council of Science Editors:

Etchebarne BE. IGF-I and leptin hormonal infusions alter the cell proliferation and transcriptional profile of the prepubertal bovine mammary gland. [Doctoral Dissertation]. Michigan State University; 2006. Available from: http://etd.lib.msu.edu/islandora/object/etd:34090

Michigan State University

25. Davis, Laurie Ellen. Mechanisms regulating parenchymal development in the bovine mammary gland.

Degree: MS, Department of Animal Science, 2002, Michigan State University

URL: http://etd.lib.msu.edu/islandora/object/etd:31853

Subjects/Keywords: Mammary glands – Growth; Heifers – Development; Epithelial cells

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APA (6^th Edition):

Davis, L. E. (2002). Mechanisms regulating parenchymal development in the bovine mammary gland. (Masters Thesis). Michigan State University. Retrieved from http://etd.lib.msu.edu/islandora/object/etd:31853

Chicago Manual of Style (16^th Edition):

Davis, Laurie Ellen. “Mechanisms regulating parenchymal development in the bovine mammary gland.” 2002. Masters Thesis, Michigan State University. Accessed March 03, 2021. http://etd.lib.msu.edu/islandora/object/etd:31853.

MLA Handbook (7^th Edition):

Davis, Laurie Ellen. “Mechanisms regulating parenchymal development in the bovine mammary gland.” 2002. Web. 03 Mar 2021.

Vancouver:

Davis LE. Mechanisms regulating parenchymal development in the bovine mammary gland. [Internet] [Masters thesis]. Michigan State University; 2002. [cited 2021 Mar 03]. Available from: http://etd.lib.msu.edu/islandora/object/etd:31853.

Council of Science Editors:

Davis LE. Mechanisms regulating parenchymal development in the bovine mammary gland. [Masters Thesis]. Michigan State University; 2002. Available from: http://etd.lib.msu.edu/islandora/object/etd:31853

Massey University

26. Hovey, Russell Charles. The role of the mammary fat pad during mammogenesis.

Degree: PhD, Animal Science, 1996, Massey University

URL: http://hdl.handle.net/10179/2623

► Development of the female mammary gland involves the proliferation and morphogenesis of epithelial cells within a matrix of adipose and connective tissue which constitutes the… (more)

Subjects/Keywords: Mammary glands; Epithelial cells; Mouse physiology; Ruminant physiology

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

APA (6^th Edition):

Hovey, R. C. (1996). The role of the mammary fat pad during mammogenesis. (Doctoral Dissertation). Massey University. Retrieved from http://hdl.handle.net/10179/2623

Chicago Manual of Style (16^th Edition):

Hovey, Russell Charles. “The role of the mammary fat pad during mammogenesis.” 1996. Doctoral Dissertation, Massey University. Accessed March 03, 2021. http://hdl.handle.net/10179/2623.

MLA Handbook (7^th Edition):

Hovey, Russell Charles. “The role of the mammary fat pad during mammogenesis.” 1996. Web. 03 Mar 2021.

Vancouver:

Hovey RC. The role of the mammary fat pad during mammogenesis. [Internet] [Doctoral dissertation]. Massey University; 1996. [cited 2021 Mar 03]. Available from: http://hdl.handle.net/10179/2623.

Council of Science Editors:

Hovey RC. The role of the mammary fat pad during mammogenesis. [Doctoral Dissertation]. Massey University; 1996. Available from: http://hdl.handle.net/10179/2623

Penn State University

27. Plichta, Kristin Ann. Mammary Epithelial Cell Subtype-Specific Analysis of Ras Pathway Activation.

Degree: 2010, Penn State University

URL: https://submit-etda.libraries.psu.edu/catalog/11251

► Breast cancers can be divided into subtypes based in part on how closely the tumor cells resemble mammary epithelial cell (MEC) subtypes resident in normal… (more)

▼ Breast cancers can be divided into subtypes based in part on how closely the tumor cells resemble mammary epithelial cell (MEC) subtypes resident in normal breast tissue. Though breast cancer subtypes differ in their aggressiveness and their response to treatment, the mechanisms by which distinct subtypes arise remain unknown. Traditionally, attempts to explain the varied clinical behavior of breast cancers rely on defining the genetic lesions harbored within individual tumors. However, recent evidence suggests that distinct breast cancer subtypes may arise from distinct MEC lineages, suggesting that some biological features of a given breast cancer subtype may be attributable to its antecedent “cell of origin”. Elucidating whether MEC lineage impacts the biology of descendant breast cancers presents a formidable challenge. By the time a tumor is clinically detectable, breast cancers have undergone clonal evolution that precludes a reliable retrospective determination of the cell of origin. As such, prospective analyses may be required to determine whether distinct MEC subtypes yield distinct cancer subtypes. We hypothesized that distinct MEC compartments yield different phenotypes in response to an identical oncogenic stimulus. To test this possibility, we generated mouse models that permit doxycycline-dependent expression of transgenes in an MEC compartment-restricted manner and developed strategies to monitor transgene-mediated phenotypes in real-time. As a first step toward studying malignant transformation of distinct MEC subtypes in mice, we tested experimental strategies designed to permit restriction of transgene expression to distinct MEC compartments in vitro. Transgenic mammary epithelium was partially disaggregated and propagated in 3D culture as mammary organoids, preserving the bilayered arrangement of the basal and luminal MEC compartments. Pairing a tet operator-driven H2B-eGFP reporter transgene with either a basal or luminal MEC transactivator enabled MEC compartment-restricted reporter gene expression. Notably, nuclear fluorescence resulting from H2B-eGFP expression enabled visualization of cellular dynamics within discrete MEC compartments. Through extended, multiparameter live cell imaging of organoids, time-lapse movies were generated that enabled visualization of MEC migration as well as tracking and quantitation of mitotic and apoptotic events. Next, we adapted this system to co-express the H2B-eGFP reporter together with a tet-operator-regulated oncogenic H-RASG12V allele. Whether expressed in a basal or luminal MEC-restricted manner, H-RASG12V expression reproducibly triggered aberrant organoid growth, reflected in measureable changes in organoid size and shape. Increases in organoid size were attributable to H-RASG12V-mediated increases in cell proliferation and decreases in cell death. In addition, H-RASG12V expression in either MEC compartment drove MECs to both traverse normal compartment boundaries and adopt modes of cellular migration distinct from those encountered in the setting… Advisors/Committee Members: Edward Joseph Gunther, Dissertation Advisor/Co-Advisor, Edward Joseph Gunther, Committee Chair/Co-Chair, Andrea Manni, Committee Member, Christopher Alan Siedlecki, Committee Member, Lisa M Shantz, Committee Member.

Subjects/Keywords: Ras; mammary organoids; breast cancer; transgenic mice; mammary epithelial cells

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

APA (6^th Edition):

Plichta, K. A. (2010). Mammary Epithelial Cell Subtype-Specific Analysis of Ras Pathway Activation. (Thesis). Penn State University. Retrieved from https://submit-etda.libraries.psu.edu/catalog/11251

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):

Plichta, Kristin Ann. “Mammary Epithelial Cell Subtype-Specific Analysis of Ras Pathway Activation.” 2010. Thesis, Penn State University. Accessed March 03, 2021. https://submit-etda.libraries.psu.edu/catalog/11251.

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

MLA Handbook (7^th Edition):

Plichta, Kristin Ann. “Mammary Epithelial Cell Subtype-Specific Analysis of Ras Pathway Activation.” 2010. Web. 03 Mar 2021.

Vancouver:

Plichta KA. Mammary Epithelial Cell Subtype-Specific Analysis of Ras Pathway Activation. [Internet] [Thesis]. Penn State University; 2010. [cited 2021 Mar 03]. Available from: https://submit-etda.libraries.psu.edu/catalog/11251.

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

Council of Science Editors:

Plichta KA. Mammary Epithelial Cell Subtype-Specific Analysis of Ras Pathway Activation. [Thesis]. Penn State University; 2010. Available from: https://submit-etda.libraries.psu.edu/catalog/11251

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

28. Atashgaran, Vahid. Hormone and transcription factor regulation of cytokines in the mammary gland.

Degree: 2018, University of Adelaide

URL: http://hdl.handle.net/2440/118007

► Increased number of menstrual cycles is associated with an increased lifetime risk for breast cancer, however the biological basis for this increased risk is not… (more)

▼ Increased number of menstrual cycles is associated with an increased lifetime risk for breast cancer, however the biological basis for this increased risk is not well understood. Previous research in mouse models suggest the immune microenvironment is critically regulated by fluctuations in circulating estrogen and progesterone across the menstrual cycle, which may affect breast cancer susceptibility. The work in this thesis aims to investigate hormonal regulation of transcription factors and cytokines that affect cells of the immune system in the mammary gland, using an array of approaches including primary human mammary epithelial organoid structures (n=6), human mammary epithelial cell lines (MCF7, T47D and ZR751), and mouse mammary gland tissues. Firstly, primary mammary epithelial organoid cultures were treated with combinations of 17-beta estradiol and progesterone for 72 hours, and the abundance of messenger RNA encoding cytokines transforming growth factor beta 1 (TGFB1), tumour necrosis factor alpha (TNFA), signal transducer and activator of transcription 3 (STAT3), STAT5, interleukin-12 (IL12), E74-like factor 5 (ELF5), C-X-C motif chemokine ligand 12 (CXCL12), S100 calcium binding protein A8 (S100A8), S100A9, Forkhead box P3 (FOXP3), and Zinc Finger E-Box Binding Homeobox 1 (ZEB1) were analysed using real-time PCR. Moreover, lentiviral vectors were used to investigate the effects of FOXP3 overexpression on downstream cytokines in the human mammary epithelial organoids. In the second approach, human mammary epithelial cell lines were treated with combinations of 17-beta estradiol and progesterone at different time courses and the abundance of mRNA encoding the cytokines of interest was analysed using real-time PCR. Further, the expression of ELF5, a mammary epithelial morphogenesis transcription factor, was transiently silenced by small interfering RNA oligos in T47D mammary epithelial cell lines to investigate the role of ELF5 in progesterone-mediated cytokine expression. Lastly, to investigate the effects of Foxp3 heterozygosity on mammary ductal morphogenesis, C57BL6 wildtype and Foxp3 heterozygous female mice were tracked over a period of 28 days by histological analysis of vaginal smears. The 4th pair of the mammary glands from each mouse was collected at each of the four stages of the cycle for cytokine expression studies and whole-mount analysis. In primary organoid cultures, there was high variability in cytokine expression between patients; the only consistent result was that combined estradiol and progesterone treatment significantly attenuated TGFB1 mRNA expression (p<0.05). Also, overexpression of FOXP3 in these cells resulted in an insignificant increase in the mRNA expression of ZEB1. Hormone treatments of cell lines at different time courses resulted in different expression of mRNA encoding the cytokines of interest. However, silencing of the ELF5 gene in T47D cells resulted in induced mRNA expression of S100A9 and CXCL12 by 50% compared to non-silenced cells (p<0.05). Finally, analysis of… Advisors/Committee Members: Ingman, Wendy (advisor), Barry, Simon (advisor), Dasari, Pallave (advisor), Adelaide Medical School (school).

Subjects/Keywords: Hormones; mammary gland; cytokines; transcription factor; mammary epithelial cells

…epithelial structures are comprised of two types of mammary epithelial cells: myoepithelial cells… …milk during lactation. These different types of mammary epithelial cells are organised… …majority of breast carcinomas originate from mammary epithelial cells (8). The stroma… …mammary epithelial cells undergo programmed cell death (i.e. apoptosis) causing the… …Review 1.4.2. CHANGES IN MAMMARY EPITHELIAL CELLS DURING THE MENSTRUAL CYCLE Fluctuations in…

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APA (6^th Edition):

Atashgaran, V. (2018). Hormone and transcription factor regulation of cytokines in the mammary gland. (Thesis). University of Adelaide. Retrieved from http://hdl.handle.net/2440/118007

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):

Atashgaran, Vahid. “Hormone and transcription factor regulation of cytokines in the mammary gland.” 2018. Thesis, University of Adelaide. Accessed March 03, 2021. http://hdl.handle.net/2440/118007.

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

MLA Handbook (7^th Edition):

Atashgaran, Vahid. “Hormone and transcription factor regulation of cytokines in the mammary gland.” 2018. Web. 03 Mar 2021.

Vancouver:

Atashgaran V. Hormone and transcription factor regulation of cytokines in the mammary gland. [Internet] [Thesis]. University of Adelaide; 2018. [cited 2021 Mar 03]. Available from: http://hdl.handle.net/2440/118007.

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

Council of Science Editors:

Atashgaran V. Hormone and transcription factor regulation of cytokines in the mammary gland. [Thesis]. University of Adelaide; 2018. Available from: http://hdl.handle.net/2440/118007

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

29. Védrine, Mégane. Rôle de l'antigène O dans la reconnaissance d'Escherichia coli par les cellules épithéliales mammaires bovines et modulation par le CD14 soluble : Sensing of escherichia coli and LPS by mammary epithelial cells is modulated by O-antigen chain and CD14.

Degree: Docteur es, Sciences de la vie et de la santé. Microbiologie, 2019, Université François-Rabelais de Tours

URL: http://www.theses.fr/2019TOUR4002

►

Les mammites constituent la première source de pertes financières des cheptels bovins laitiers en France et dans le monde. Parmi les agents pathogènes des infections… (more)

Subjects/Keywords: Lipopolysaccharide; Mastitis; Escherichia coli; O-antigen; Mammary epithelialcells; Rough-LPS; Smooth-LPS; CD14; Mammary epithelial cells; Rough LPS; Smooth Lipopolysaccharide; CD14 antigen

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

APA (6^th Edition):

Védrine, M. (2019). Rôle de l'antigène O dans la reconnaissance d'Escherichia coli par les cellules épithéliales mammaires bovines et modulation par le CD14 soluble : Sensing of escherichia coli and LPS by mammary epithelial cells is modulated by O-antigen chain and CD14. (Doctoral Dissertation). Université François-Rabelais de Tours. Retrieved from http://www.theses.fr/2019TOUR4002

Chicago Manual of Style (16^th Edition):

Védrine, Mégane. “Rôle de l'antigène O dans la reconnaissance d'Escherichia coli par les cellules épithéliales mammaires bovines et modulation par le CD14 soluble : Sensing of escherichia coli and LPS by mammary epithelial cells is modulated by O-antigen chain and CD14.” 2019. Doctoral Dissertation, Université François-Rabelais de Tours. Accessed March 03, 2021. http://www.theses.fr/2019TOUR4002.

MLA Handbook (7^th Edition):

Védrine, Mégane. “Rôle de l'antigène O dans la reconnaissance d'Escherichia coli par les cellules épithéliales mammaires bovines et modulation par le CD14 soluble : Sensing of escherichia coli and LPS by mammary epithelial cells is modulated by O-antigen chain and CD14.” 2019. Web. 03 Mar 2021.

Vancouver:

Védrine M. Rôle de l'antigène O dans la reconnaissance d'Escherichia coli par les cellules épithéliales mammaires bovines et modulation par le CD14 soluble : Sensing of escherichia coli and LPS by mammary epithelial cells is modulated by O-antigen chain and CD14. [Internet] [Doctoral dissertation]. Université François-Rabelais de Tours; 2019. [cited 2021 Mar 03]. Available from: http://www.theses.fr/2019TOUR4002.

Council of Science Editors:

Védrine M. Rôle de l'antigène O dans la reconnaissance d'Escherichia coli par les cellules épithéliales mammaires bovines et modulation par le CD14 soluble : Sensing of escherichia coli and LPS by mammary epithelial cells is modulated by O-antigen chain and CD14. [Doctoral Dissertation]. Université François-Rabelais de Tours; 2019. Available from: http://www.theses.fr/2019TOUR4002

Indian Institute of Science

30. Kumar, Hindupur Sravanth. Stress Signaling In Development And Carcinogenesis : Role Of AMP-Activated Protein Kinase.

Degree: PhD, Faculty of Science, 2013, Indian Institute of Science

URL: http://etd.iisc.ac.in/handle/2005/2189

► Rapidly growing tumor cells outgrow their blood supply resulting in a microenvironment with reduced oxygen and nutrients. Using an in vitro transformation model we found… (more)

▼ Rapidly growing tumor cells outgrow their blood supply resulting in a microenvironment with reduced oxygen and nutrients. Using an in vitro transformation model we found that cancer cells expressing the SV40 ST antigen (+ST cells) are more resistant to glucose deprivation-induced cell death than cells lacking the SV40 ST antigen (−ST cells). Mechanistically, we found that the ST antigen mediates this effect by activating a nutrient-sensing kinase, AMP-activated protein kinase (AMPK). We further show that AMPK mediates its effects, at least in part, by inhibiting mTOR (mammalian target of rapamycin), thereby shutting down protein translation, and by inducing autophagy as an alternate energy source. Resistance to anoikis upon anchorage-deprivation is yet another form of stress tolerated by both normal stem/progenitor cells of various tissues in our body and by cancer cells. Using mammospheres as a model to enrich for stem/progenitor cells we found that mammosphere formation is accompanied with increased activation of AMPK. Concomitant with AMPK activation, we detected increased phosphorylation of the anti-apoptotic protein PED/PEA15. We further demonstrate that AMPK directly interacts with and phosphorylates PEA15 at Ser116, thus establishing PEA15 as a new AMPK target. Thus, our study has identified AMPK-PEA15 signaling as a key component of sphere formation by both normal and cancerous breast tissues. During metastasis, epithelial cells lose attachments to their neighbors, acquire a mesenchymal-like morphology, a process termed as epithelial-mesenchymal transition (EMT) and become motile. Our results indicate that AMPK regulates EMT by both transcriptional and post-translational modification of EMT-inducing transcription factor, Twist. Thus, our study has identified a role for AMPK in nutrient deprivation, anchorage-independent growth, and epithelial-mesenchymal transition involved in metastasis. In addition, we have identified two novel substrates of AMPK, PEA15 and Twist, that may play key roles in cancer progression. Thus, our study suggests that targeting AMPK, or its newly identified substrates, can be explored as possible anti-cancer mechanisms. Advisors/Committee Members: Rangarajan, Annapoorni (advisor).

Subjects/Keywords: Carcinoma Protein; Protein Kinase; AMP-Activated Protein Kinase; Autophagy; Metastasis; Epithelial-Mesenchymal Transition; Carcinogenesis; AMPK Signaling; AMPK Phosphorylates; Human Mammary Epithelial Cells; Molecular Biology

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

APA (6^th Edition):

Kumar, H. S. (2013). Stress Signaling In Development And Carcinogenesis : Role Of AMP-Activated Protein Kinase. (Doctoral Dissertation). Indian Institute of Science. Retrieved from http://etd.iisc.ac.in/handle/2005/2189

Chicago Manual of Style (16^th Edition):

Kumar, Hindupur Sravanth. “Stress Signaling In Development And Carcinogenesis : Role Of AMP-Activated Protein Kinase.” 2013. Doctoral Dissertation, Indian Institute of Science. Accessed March 03, 2021. http://etd.iisc.ac.in/handle/2005/2189.

MLA Handbook (7^th Edition):

Kumar, Hindupur Sravanth. “Stress Signaling In Development And Carcinogenesis : Role Of AMP-Activated Protein Kinase.” 2013. Web. 03 Mar 2021.

Vancouver:

Kumar HS. Stress Signaling In Development And Carcinogenesis : Role Of AMP-Activated Protein Kinase. [Internet] [Doctoral dissertation]. Indian Institute of Science; 2013. [cited 2021 Mar 03]. Available from: http://etd.iisc.ac.in/handle/2005/2189.

Council of Science Editors:

Kumar HS. Stress Signaling In Development And Carcinogenesis : Role Of AMP-Activated Protein Kinase. [Doctoral Dissertation]. Indian Institute of Science; 2013. Available from: http://etd.iisc.ac.in/handle/2005/2189

Open Access Theses and Dissertations