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目的探讨17β雌二醇(E2)、他莫昔芬(TAM)和雷洛昔芬(RAL)对前列腺癌PC3凋亡、细胞周期的影响及作用机制。方法检测不同浓度E2、TAM、RAL作用于PC3细胞不同时间后细胞生长抑制率和48 h后细胞周期分布、凋亡率、bcl-2和Caspase-3蛋白的表达,以及12 h后p21WAF1 mRNA．表达。Hoechst染色和电镜观察细胞凋亡。结果E2、TAM、RAL呈时间及浓度依赖性抑制PC3细胞增殖。10-4 mol／L E2、10-5 mol／L TAM和10-5 mol／L RAL作用48 h后检测到凋亡,凋亡率分别为(21．54±0．91)％、(38．28±1．16)％、(42．41±2．26)％(P<0．05),bcl-2和Caspase-3分别为对照组的0．5、0．4、0．35倍;1．4、1．6、1．6倍。细胞阻滞在G1期。对照组和处理组p21WAF1基因表达强度分别为1．12、3．31、5．24、4．48。结论E2、TAM、RAL可以增强p21WAF1基因表达使PC3阻滞于G1期,通过下调bcl-2蛋白并上调Caspase-3蛋白诱导PC3凋亡。
Objective To investigate the effects of 17β estradiol (E2), tamoxifen (TAM) and raloxifene (RAL) on apoptosis and cell cycle of PC3 in prostate cancer and its mechanism. Methods The cell growth inhibitory rate and the cell cycle distribution, apoptosis rate, bcl-2 and Caspase-3 protein expression after different concentrations of E2, TAM and RAL were tested at different time points and 48 hours after exposure. expression. Hoechst staining and electron microscopy were used to observe apoptosis. Results E2, TAM and RAL inhibited the proliferation of PC3 cells in a time and concentration dependent manner. Apoptosis was detected after treated with 10-4 mol / L E2, 10-5 mol / L TAM and 10-5 mol / L RAL for 48 h, respectively. The apoptotic rates were (21.54 ± 0.91)% and (28.41 ± 2.26)% (P <0.05). The expressions of bcl-2 and caspase-3 in the control group were 0.5, 0.4 and 0.35 Times; 1.4,1.6,1.6 times. Cell arrest in G1 phase. The expression intensity of p21WAF1 gene in control group and treatment group were 1.12,3.31,5.24,4.48 respectively. Conclusion E2, TAM and RAL can enhance the expression of p21WAF1 and make PC3 arrest in G1 phase. PC3 apoptosis can be induced by down-regulating bcl-2 protein and up-regulating Caspase-3 protein.