中文摘要：

目的观察米非司酮在体外诱导前列腺癌PC-3细胞凋亡的作用机制以及Akt激酶在前列腺癌生长过程中的作用。方法采用Westernblot方法检测不同前列腺癌细胞株癌细胞以及米非司酮作用后PC-3细胞中Akt蛋白磷酸化后蛋白含量，以及相关蛋白的表达量。结果前列腺癌PC-3细胞中Akt磷酸化后蛋白即[p-Akt（Thr^308）和p-Akt（Ser^473）]的含量明显高于激素依赖性前列腺癌LNCaP细胞中的蛋白表达量，其表达量分别为0．27±0．05和0．22±0．07；O．46±0．09和0．37±0．10（P〈0．05）。10μmol／L米非司酮作用于PC-3细胞后p-Akt（Thr^308）和p-Akt（Ser^473）磷酸化蛋白的含量均明显下降，但其中p-Akt（nr3。）蛋白表达量变化尤为显著，4～24h4个时间组蛋白含量分别为0．24±0．08、0．11±0．03、0．05±0．01和0．01±0．00；其蛋白表达量下降速度较p-Akt（Ser^473）快且显著，p-Akt（Serg7。）磷酸化蛋白4～24h4个时间组蛋白含量分别为0．56±0．17、0．42＋0．11、0．28±0．09和0．12±0．05。米非司酮作用于PC-3细胞后使Caspase-9、Caspase-3被激活裂解出有活性的激活片段。结论Akt激酶在前列腺癌生长、发展以及激素依赖性向激素非依赖性的转变过程中起着重要作用。p-Akt（Thr^308）蛋白磷酸化水平在Akt磷酸化激活过程中占主导地位，是Akt激活的必要过程。米非司酮抑制前列腺癌PC-3细胞的增殖，诱导细胞凋亡，其可能是通过抑制Akt信号转导通路，从而激活Caspase。

英文摘要：

Objective To investigate the cell apoptosis induced by mifepristone in prostate carcinoma cell line PC-3 and the mechanisms involved. Methods Western blotting analysis was used to detect Akt phosphorylation and associated protein expression in different prostate cancer cell line ceils and PC-3 cells treated with mifepristone. Results In PC-3 cells, Akt phosphorylation, that was p-Akt （Thr^308 ） and p-Akt （ Ser^473 ）, was significantly higher than the hormone-dependent prostate cancer LNCaP ceils, and their expression levels were respectively 0. 27 ±0. 05 and 0. 22 ±0. 07, 0. 46 ±0. 09 and 0. 37 ±0. 10 （P 〈 0. 05）. The p-Akt （Thr^308） and p-Akt （Ser473） phosphorylation in PC-3 cells treated with 10 μmol/L mife- pristone was significantly decreased. The p-Akt （Thr^308 ） phosphorylation was particularly marked, its expression was respectively 0. 24 ± 0.08, 0. 11 ± 0. 03, 0. 05 ± 0. 01 and 0. 01 ± 0. 00 during 4-24 h, and declined rapidly as compared with the p-Akt （ Ser473 ） phosphorylation which expression levels were respectively 0. 56 ±0. 17, 0. 42 ±0. 11,0. 28 ±0. 09 and 0. 12 ±0.05 during 4-24 h. Caspase-9 and easpase-3 were activated into cleavage fragment in the PC-3 eells treated with mifepristone. Conclusion Akt kinase plays an important role in prostate cancer growth, development and hormone-dependent to hormone-inde- pendent transformation. The p-Akt （ Thr^308 ） phosphorylation, which plays a dominant role in Akt phospho- rylation, is necessary in the course of Akt activation. Mifepristone inhibits prostate cancer PC-3 cell proliferation and induces apoptosis by suppressing the Akt signal transduetion pathway and activating caspase.