EFFECTS AND MECHANISMS OF ENDOSTATIN ON THE GROWTH OF OVARIAN CANCER SKOV_3 CELLS IN VITRO AND IN VI

来源 :Chinese Journal of Cancer Research | 被引量 : 0次 | 上传用户:ckxworkman
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Objective: To evaluate the inhibitory effect of Endostatin on ovarian cancer cell line SKOV3 and to investigate the possible mechanism of the inhibition. Methods: Using MTT, transmission electron microscope (TEM) and immunocytochemistry, the effects of Endostatin on the proliferation of SKOV3 cells were studied. Nude mice were subcutaneously implanted with SKOV3 cells. The cell apoptosis of implanted tumor was detected by TUNEL and TEM. The expressions of bcl-2 and bax in implanted tumor tissues were measured by RT-PCR and immunohistochemistry. Results: Endostatin significantly inhibited the proliferation of SKOV3 cells in vitro (P<0.01) and induced cell apoptosis, whereas the expressions of bcl-2 and bax were not changed obviously in SKOV3 cell treated with Endostatin. The mean tumor weight of Endostatin treated group was markedly lower than that of PBS control group (P<0.05). The expression of bcl-2 was down-regulated in Endostatin treated group, but bax was not influenced. Conclusions: The results demonstrated that Endostatin might have anti-tumor effect on ovarian carcinoma. One of the important mechanisms of Endostatin effect of anti-angiogenic and anti-tumor activities might involve regulating the bcl-2/bax expression and inducing apoptosis. Objective: To evaluate the inhibitory effect of Endostatin on ovarian cancer cell line SKOV3 and to investigate the possible mechanism of the inhibition. Methods: Using MTT, transmission electron microscope (TEM) and immunocytochemistry, the effects of Endostatin on the proliferation of SKOV3 cells were The cell apoptosis of implanted tumor was detected by TUNEL and TEM. The expressions of bcl-2 and bax in implanted tumor tissues were measured by RT-PCR and immunohistochemistry. Results: Endostatin was implanted with SKOV3 cells. the proliferation of SKOV3 cells in vitro (P <0.01) and induced cell apoptosis, while the expressions of bcl-2 and bax were not changed obviously in SKOV3 cell treated with Endostatin. The mean tumor weight of Endostatin treated group was markedly lower than that that of PBS control group (P <0.05). The expression of bcl-2 was down-regulated in Endostatin treated group, but bax was not influenced. Conclusio ns: The results characterized that Endostatin might have anti-tumor effect on ovarian carcinoma. One of the important mechanisms of Endostatin effect of anti-angiogenic and anti-tumor activities might involve regulating the bcl-2 / bax expression and inducing apoptosis.
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