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孕酮和米非司酮对前列腺癌PC-3细胞作用机理的研究 被引量:2

Mechanism of the effects of progesterone and mifepristone on human prostate cancer PC-3 cells
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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。Westernblot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7d,孕酮(100nmol/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(10μmol/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。 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.
出处 《中华泌尿外科杂志》 CAS CSCD 北大核心 2006年第5期349-351,共3页 Chinese Journal of Urology
基金 国家自然科学基金资助项目(30471731)
关键词 米非司酮 孕酮 前列腺肿瘤 细胞外信号调节激酶 Mifepristone Progesterone Prostatic neoplasms Carcinoma Extraeellular signal-regulated kinase
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