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The role of adherens junction proteins in the initiation of ovarian cancer Wu, Colleen
Abstract
Cells of the human ovarian surface epithelium (OSE) are plastic and uncommitted. Specifically, OSE cells do not express E-cadherin and they can shift between epithelial and stationary or mesenchymal and migratory phenotypes. In contrast, well differentiated, low grade ovarian carcinomas, which are thought to arise from the OSE, express E-cadherin and they display a committed epithelial phenotype. E-cadherin expression and stationary epithelial commitment are first observed in OSE-derived inclusion cysts and clefts which are thought to be weakly pre-neoplastic. Therefore, I determined if forced E-cadherin expression in OSE cells was capable of inducing this commitment to a stationary epithelial phenotype that is a hallmark of the earliest stages of ovarian carcinoma formation. High levels of forced E-cadherin expression in an immortalized human OSE cell line achieved by stable transfection induced the localization of E-cadherin, P-catenin, and f-actin to sites of cell-cell contact. High levels E-cadherin also resulted in an increase in the amount of P-catenin associated with the cytoskeleton formation and a decrease in LEF-l/p-catenin signaling. Taken together, these data indicate that high levels of forced E-cadherin expression induced the formation of functional epithelial junctions in immortalized OSE cells. In addition, these cells had migratory capabilities in threedimensional basement membrane gels compared to controls and low E-cadherin expressors. This strongly suggests that E-cadherin is capable of inducing a stationary epithelial phenotype in human OSE cells.
Item Metadata
Title |
The role of adherens junction proteins in the initiation of ovarian cancer
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Creator | |
Publisher |
University of British Columbia
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Date Issued |
2002
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Description |
Cells of the human ovarian surface epithelium (OSE) are plastic and
uncommitted. Specifically, OSE cells do not express E-cadherin and they can shift
between epithelial and stationary or mesenchymal and migratory phenotypes. In contrast,
well differentiated, low grade ovarian carcinomas, which are thought to arise from the
OSE, express E-cadherin and they display a committed epithelial phenotype. E-cadherin
expression and stationary epithelial commitment are first observed in OSE-derived
inclusion cysts and clefts which are thought to be weakly pre-neoplastic. Therefore, I
determined if forced E-cadherin expression in OSE cells was capable of inducing this
commitment to a stationary epithelial phenotype that is a hallmark of the earliest stages of
ovarian carcinoma formation.
High levels of forced E-cadherin expression in an immortalized human OSE cell
line achieved by stable transfection induced the localization of E-cadherin, P-catenin, and
f-actin to sites of cell-cell contact. High levels E-cadherin also resulted in an increase in
the amount of P-catenin associated with the cytoskeleton formation and a decrease in
LEF-l/p-catenin signaling. Taken together, these data indicate that high levels of forced
E-cadherin expression induced the formation of functional epithelial junctions in
immortalized OSE cells. In addition, these cells had migratory capabilities in threedimensional
basement membrane gels compared to controls and low E-cadherin
expressors. This strongly suggests that E-cadherin is capable of inducing a stationary
epithelial phenotype in human OSE cells.
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Extent |
7997356 bytes
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Genre | |
Type | |
File Format |
application/pdf
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Language |
eng
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Date Available |
2009-09-22
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Provider |
Vancouver : University of British Columbia Library
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Rights |
For non-commercial purposes only, such as research, private study and education. Additional conditions apply, see Terms of Use https://open.library.ubc.ca/terms_of_use.
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DOI |
10.14288/1.0090542
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URI | |
Degree | |
Program | |
Affiliation | |
Degree Grantor |
University of British Columbia
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Graduation Date |
2002-11
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Campus | |
Scholarly Level |
Graduate
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Aggregated Source Repository |
DSpace
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Item Media
Item Citations and Data
Rights
For non-commercial purposes only, such as research, private study and education. Additional conditions apply, see Terms of Use https://open.library.ubc.ca/terms_of_use.