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目的:研究坦索罗辛对前列腺癌PC-3细胞增殖与凋亡的影响。方法:以0(空白对照组)、12.5、25、50μmol/L坦索罗辛(坦索罗辛低、中、高浓度组)作用于PC-3细胞48 h后,通过MTT法检测细胞活力,Hoechst 33258染色检测细胞凋亡率,Western blot法检测核糖体Bax、B淋巴细胞瘤2(Bcl-2)蛋白表达及蛋白激酶B(Akt)、哺乳动物雷帕霉素靶蛋白(m TOR)、S6蛋白激酶(p70S6K)、4E结合蛋白1(4E-BP1)的磷酸化水平。结果:与空白对照组比较,坦索罗辛低、中、高浓度组PC-3细胞活力和Akt、p70S6K、4E-BP1磷酸化水平均降低,Bax蛋白表达水平升高(P<0.05或P<0.01);坦索罗辛中、高浓度组PC-3细胞的凋亡率升高,Bcl-2蛋白表达和m TOR磷酸化水平降低(P<0.01),上述效果均呈浓度依赖性。结论:坦索罗辛能抑制前列腺癌PC-3细胞增殖并诱导其凋亡,其机制可能与抑制Akt/m TOR信号通路激活有关。
Objective: To study the effect of tamsulosin on the proliferation and apoptosis of prostate cancer PC-3 cells. Methods: PC-3 cells were treated with 0 (blank control), 12.5,25 and 50 μmol / L tamsulosin (low, medium and high concentrations of tamsulosin) for 48 h, and cell viability Hoechst 33258 staining was used to detect the apoptosis rate. Western blot was used to detect the expression of Bax, Bcl-2 and Akt in mammals, and the mTOR of mammalian target protein (mTOR) , S6 protein kinase (p70S6K), 4E binding protein 1 (4E-BP1). RESULTS: Compared with the blank control group, the phosphorylation levels of Akt, p70S6K and 4E-BP1 in the tamsulosin low, middle and high concentration groups were decreased and the protein expression of Bax was increased (P <0.05 or P <0.01). The apoptosis rates of tamsulosin in medium and high concentrations of PC-3 cells were increased, the expression of Bcl-2 protein and phosphorylation of mTOR decreased (P <0.01), and the above effects were in a concentration-dependent manner. Conclusion: Tamsulosin can inhibit the proliferation and induce the apoptosis of PC-3 cells, which may be related to the inhibition of Akt / m TOR signaling pathway.