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The role of adherens junction proteins in the initiation of ovarian cancer Wu, Colleen


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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