PXD101诱导人前列腺癌细胞PC3凋亡的线粒体信号通路

目的:探讨PXD101(又称belinostat)诱导人前列腺癌PC3细胞凋亡的线粒体通路。方法:PXD101以不同刺激时间和剂量处理PC3细胞,CCK-8法检测细胞的活力;流式细胞术检测细胞的凋亡率和线粒体膜电位;Western blot检测线粒体凋亡相关蛋白Bcl-2、细胞色素C(Cyt C)和Bax;caspase-3活性检测试剂盒检测caspase-3活性。结果:PXD101能以时间和剂量依赖的方式抑制PC3细胞的存活(P0.05),流式细胞术检测结果表明PXD101处理后PC3细胞的凋亡率明显增加(P0.01)。PXD101能时间依赖性致线粒体膜电位降低和Bcl-2蛋白含量明显下降,Bax蛋白含量上升,促进线粒体释放Cyt C蛋白,caspase-3活性明显增强。结论:PXD101通过线粒体途径诱导人前列腺癌细胞系PC3细胞凋亡。

PXD101 induces apoptosis of human prostate cancer cell line PC3 by mitochondrial signal pathway

AIM: To explore the mitochondrial pathway in the apoptosis of PC3 cells induced by PXD101 (also named as belinostat).METHODS: PC3 cells were treated with PXD101 at different doses or stimulated with PXD101 for different time. The effect of PXD101 on the viability of PC3 cells was measured by CCK-8 assay. The apoptotic rates and the mitochondrial membrane potential (MMP) were analyzed by flow cytometry. The protein levels of Bcl-2, Bax and cytochrome C (Cyt C) were determined by Western blot. The caspase-3 activity were tested by caspase-3 activity assay kit.RESULTS: The viability of the PC3 cells was inhibited by PXD101 in a dose-and time-dependent manner. Flow cytometric analysis showed that the apoptotic rates were increased in the cells treated with PXD101 (P<0.01). At the same time, PXD101 induced the decreases in MMP and Bcl-2, the release of Cyt C, and the increase in caspase-3 activity.CONCLUSION: PXD101 induces the apoptosis of human prostate cancer cell line PC3 by mitochondrial signal pathway.