Regulation Of Progesterone On Bcl-2 Expression In Ovarian CancerCell Line

Ovarian carcinoma is one of the most common fatal gynecologic malignancies in the word .the incidence of this disease rises after women reach menopause due to lower levels of sex steroids.some research demonstrate that the risk may be reduced by use of combination-type oral contraceptives(COCS),which contain estrogen and a high dose of progesterone.in addition ,progesterone has been used in the clinical treatment of ovarian carcinomas.However,the molecular mechanism of the anticancer effect of progesterone is not yet fully understood.so my trial is to proceed a deep research in order to provide a base for chemoprevention and treatment against ovarian cancer. Objective: To investigate the regulatory effect of progesterone on proliferation and apoptosis in ovarian cancer cell line HO-8910 in vitro.Method: Ovarian cancer cell line HO-8910 originated from human ovarian serous cystadenocarcinoma was cultured in vitro. two group were set up:study group(progesterone in different concentrations)and control group without progesterone.cell proliferation was measured by 3-(4.5-dimethylthiazol-z-yl)-2.5-dipheny tertrazolium blue (MTT) colorimetric assay.celL apoptotic percentage were detected by flow cytometry.in addition express -ion of intracellular bcl-2 gene was analyzed by RT-PCR. Result: Progesterone of 1×10-7～1×10-5mol/L inhibited HO-8910 cell growth significantly in a dose dependent manner(P<0.01),after treatment with progesterone for 24h, 48h, 72h. When the concentation of progesterone were 1×10-7～1×10-5mol/L and after action for 72h, the percentage of apoptosis were 14.67% ,26.96% ,78.55%.It has a significant difference compared with control group(P<0.01).Analysis on the expression of intracellular bcl-2 gene,After treated at concentration of 1×10-5mol/L expression of bcl-2 gene was down regulated .Conclutions: It is suggested that progesterone can inhibit the proliferation of epithelial ovarian cancer cells in vitro and there is an accordant dose-response relationshop.Its anticancer effect seems to be due to induction of apoptosis which maybe a result of dowm-regulation of the anti-apoptotic gene bcl-2.