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首页> 外文期刊>Cancer Biology >Ahmed Gafar, Mohammed Bashandy, Sayed Bakry, Mahmoud A. Khalifa, and Walid Abu Shair
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Ahmed Gafar, Mohammed Bashandy, Sayed Bakry, Mahmoud A. Khalifa, and Walid Abu Shair

机译:艾哈迈德·贾法尔,穆罕默德·巴申德,赛义德·巴克里,马哈茂德A.哈利法与瓦尔德·阿布·谢尔(Walid Abu Sher)

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Lithocholic acid (LCA) is toxic to human prostate cancer cells. We previously studied the effects of LCA on cell viability, cell proliferation and mitochondrial function in LNCaP and PC-3 prostate cancer cell lines. In the present study, we investigated the induction of extrinsic apoptosis by LCA in androgen independent PC-3 and DU-145 cells. In PC-3 and DU-145 cells, LCA triggered extrinsic apoptosis pathways and induced typical extrinsic apoptosis -related proteins, such TRIAL, FasL, FADD, DR5, DR4 and Cleaved caspase8. Treatment of prostate cancer cells with IETD AFC (10 μM), an inhibitor of Caspase 8 partially inhibited apoptosis that induced by LCA. Also, we found Death receptor (DR5) silencing partially Blocked LCA to induced cell death. Collectively, these results indicate that extrinsic apoptosis induced by LCA in PC-3 and DU-145 play a secondary role in cell death and there might be another cell surface receptor that LCA triggers to induce cell death.
机译:胆酸(LCA)对人前列腺癌细胞有毒性。我们先前研究了LCA对LNCaP和PC-3前列腺癌细胞系中细胞活力,细胞增殖和线粒体功能的影响。在本研究中,我们研究了LCA在雄激素非依赖性PC-3和DU-145细胞中诱导外源性凋亡的过程。在PC-3和DU-145细胞中,LCA触发了外在凋亡通路并诱导了典型的外在凋亡相关蛋白,例如TRIAL,FasL,FADD,DR5,DR4和Casped Caspase8。 Caspase 8抑制剂IETD AFC(10μM)对前列腺癌细胞的治疗部分抑制了LCA诱导的细胞凋亡。此外,我们发现死亡受体(DR5)使部分LCA沉默从而导致细胞死亡。总体而言,这些结果表明,LCA在PC-3和DU-145中诱导的外在凋亡在细胞死亡中起次要作用,并且可能还有另一种细胞表面受体被LCA触发以诱导细胞死亡。

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