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E-cadherin promotes proliferation of human ovarian cancer cells in vitro via activating MEK/ERK pathway

	author = {Ling-ling Dong and Lian Liu and Chun-hong Ma and Ji-sheng Li and Chao Du and Shan XU and Li-hui Han and Li Li and Xiu-wen Wang},
	title = {E-cadherin promotes proliferation of human ovarian cancer cells in vitro via activating MEK/ERK pathway},
	journal = {Acta Pharmacologica Sinica},
	volume = {33},
	number = {6},
	year = {2016},
	keywords = {},
	abstract = {Aim: E-cadherin is unusually highly expressed in most ovarian cancers. This study was designed to investigate the roles of E-cadherin in the carcinogenesis and progression of ovarian cancers.
 Methods: Human ovarian adenocarcinoma cell line SKOV-3 was examined. E-cadherin gene CDH1 in SKOV-3 cells was knocked down via RNA interference (RNAi), and the resultant variation of biological behavior was observed using CCK-8 and colony formation experiment. E-cadherin-mediated Ca2+-dependent cell-cell adhesion was used to study the mechanisms underlying the effects of E-cadherin on the proliferation and survival of SKOV-3 cells. The expression levels of E-cadherin, extracellular signal-related kinase (ERK), phosphorylated ERK (P-ERK) were measured using Western blot assays.
 Results: Transfection with CDH1-siRNA for 24–96 h significantly suppressed the growth and proliferation of SKOV-3 cells. E-cadherin-mediated calcium-dependent cell-cell adhesion of SKOV-3 cells resulted in a rapid increase of P-ERK, but did not modify the expression of ERK protein. The phosphorylation of ERK in the cells was blocked by pretreatment with the MEK1 specific inhibitor PD98059 (50 μmol/L), but not by the PI3K inhibitor wortmannin (1 μmol/L) or PKA inhibitor H89 (10 μmol/L).
 Conclusion: E-cadherin may function as a tumor proliferation enhancer via activating the MEK/ERK pathway in development of ovarian epithelial cancers.},
	issn = {1745-7254},	url = {}