地塞米松抑制卵巢癌HO-8910细胞增殖机制的研究

Mechanism of inhibition of proliferation by Dexamethasone in an ovarian cancer cell line HO-8910

目的 探讨地塞米松 (dexamethasone ,Dex)抑制人卵巢癌HO -8910细胞增殖的可能机制。方法 采用细胞计数法检测细胞增殖、流式细胞术测定细胞周期 ,同位素掺入半定量RT -PCR检测细胞周期蛋白依赖性激酶抑制剂p2 1/WAF1的表达水平。结果 Dex诱导HO -8910细胞发生G0 /G1期停滞 ,使p2 1/WAF1mRNA表达上调 ;糖皮质激素受体拮抗剂RU486可逆转细胞增殖和p2 1/WAF1表达的变化。结论 Dex对HO -8910细胞增殖的抑制可能与诱导p2 1/WAF1表达有关。

Objective To investigate the possible mechanism of the growth-inhibitory effect of dexamethasone on a human ovarian cancer cell line HO-8910. Methods The effect of dexamethasone on proliferation of HO-8910 cells was assessed by cell counts. Cell cycle was examined by flow cytomery, and the expression of cyclin-dependent kinase inhibitor p21/WAF1 was analyzed by semi-quantative RT-PCR. Results Dexamethasone induced G0/G1 arrest of HO-8910 cells and increased the expression of p21/WAF1 mRNA. RU486, an antagonist of glucocorticoid receptor, reversed the changes of cell proliferation and p21/WAF1 expression in HO-8910 cells. Conclusion Increase of p21/WAF1 mRNA expression may involve in the proliferation-inhibition of HO-8910 cells by Dex.