中文摘要：

目的 探讨孕酮和米非司酮促进前列腺癌PC-3细胞增殖作用的机理.方法 细胞培养观察孕酮和米非司酮对前列腺癌PC-3细胞增殖的影响.RT-PCR检测PC-3细胞孕激素受体mRNA的表达.Western blot检测孕酮对PC-3细胞细胞外信号调节激酶ERK1/2活性的影响,并观察米非司酮对孕酮的阻断效果.结果 细胞培养7 d,孕酮（100 nmol/L）组细胞数量为（3.2±0.3）×105,明显高于正常培养组[（1.9±0.2）×105]（P＜0.05）;米非司酮（10 μmol/L）组为（1.3±0.2）×105,明显低于正常培养组（P＜0.05）.PC-3细胞有孕激素受体mRNA的表达.孕酮可以激活ERK1/2,而米非司酮阻断孕酮对ERK1/2的激活,孕酮组与孕酮＋米非司酮组p-ERK1/2条带强度差异有统计学意义（吸光度A值分别为70752±16377和12493±3478,P＜0.05）.结论 孕酮对PC-3细胞的促进增殖作用与激活细胞ERK1/2有关;米非司酮阻断孕酮对PC-3细胞ERK1/2的活化,从而抑制细胞增殖.

英文摘要：

Objective To explore the mechanism of the effects of progesterone and mifepristone on PC-3 prostate cancer cells. Methods Ceil proliferation assays were performed to demonstrate the effects of progesterone and mifepristone on PC-3 cells. Expression of progesterone receptor gene mRNA was detected by reverse transcriptase-polymerase chain reaction （RT-PCR） in PC-3 ceils. Western blot analysis was employed to show the effects of progesterone and mifepristone on phosphoryiation of extracellular signal-regulated kinase 1/2 （ERK1/2） in PC-3 cells. Results After 7-d culture, the cell proliferation were significantly different between normal culture group and drug treatment group （ P 〈 0.05 ）. The cell number was （ 1.9 ± 0.2）× 10^5 , （3.2± 0. 3） × 10^2 and （ 1.3 ± 0.2） ×10^5 ,respectively,in normal culture group ,progesterone （100 nmol/L） group and mifepristone （10 μmol/L） group. RT-PCR showed obvious expression of progesterone receptor mRNA in PC-3 cells. Western blot showed that phosphoryiated （activated） form of ERK1/2 was improved shortly？ after progesterone added to PC-3 cells. This effect was blocked by mifepristone （10μmoi/L） added 1 h before progesterone stimulation. The intensity of p-ERK1/2 band in progesterone and mifepristone groups was 70752 ± 16377 and 12493 ± 3478, respectively （ P 〈 0.05 ）. Conclusions Progesterone can improve PC-3 ceil proliferation by activation of ERK1/2 pathway;mifepristone can inhibit PC-3 cell proliferation by blockage of progesterone effects on ERK1/2 activation.