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All-trans Retinoic Acid On Human Ovarian Cancer Cell Lines Coc1 Proliferation Differentiation And Apoptosis

Posted on:2005-05-26Degree:MasterType:Thesis
Country:ChinaCandidate:M YangFull Text:PDF
GTID:2204360122490140Subject:Pathology and pathophysiology
Abstract/Summary:PDF Full Text Request
Objective: To investigate the effects of all-trans retinoic acid (ATRA) on prolifetation and differentiation in ovarian cancer cell line COC1 in vitro. Methods: Human ovarian cancer cell line COC1 was cultured in medium containing ATRA in different concentrations in vitro. Cell proliferation inhibition was tested by MTT assay. The cell cycle was analyzed by flow cytometry(FCM) system. Morphological changes of cell differentiation were observed by light and transmission electron microscopy, and the expression of Ki-67 in cancer cells were measured with immunocytochemistry. In addition, CA125 expression in the culture medium was measured by ELISA. Result: ①ATRA of 10-7~10-5mol/L inhibited COC1 cell proliferation significantly in a dose-dependent and time-dependent manner (p<0.01). ②With the increase of ATRA concentrations, the number of cells in G0/G1 phase were elevated from 31.34% to 56.92%,and the number of cells in S phase were obviously decreased from 58.50% to 32.71%.It suggested that ATRA could arrest the cell cycle at G1/S checkpoint.③By light and transmission electron microscopy, COC1 cells after treated by ATRA showed striking morphological characteristics of differentiation. ④.The expression of Ki-67 was decreased in COC1 after ATRA treatment.⑤ATRA could also suppress the expression of CA125 tumor marker in COC1 cells with a dose-dependent, which was positively correlated to the expression of Ki-67. Conclusion: ATRA can both inhibit proliferation and induce differentiation of human ovarian cancer cell line COC1. These results may provide an effective and novel approach for clinical treatment of human ovarian cancer.
Keywords/Search Tags:Ovarian neoplasms, Retinoic acid, Proliferation, Differentiation
PDF Full Text Request
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