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首页> 外文期刊>Apoptosis >Calyculin A causes sensitization to tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-induced apoptosis by ROS-mediated down-regulation of cellular FLICE-inhibiting protein (c-FLIP) and by enhancing death receptor 4 mRNA stabilization
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Calyculin A causes sensitization to tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-induced apoptosis by ROS-mediated down-regulation of cellular FLICE-inhibiting protein (c-FLIP) and by enhancing death receptor 4 mRNA stabilization

机译：Calyculin A通过ROS介导的细胞FLICE抑制蛋白（c-FLIP）的下调和增强死亡受体4 mRNA的稳定作用，导致对肿瘤坏死因子相关的凋亡诱导配体（TRAIL）诱导的凋亡的敏感性

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摘要

Calyculin A (Cal A) is a serine/threonine phosphatase inhibitor that is capable of inducing apoptosis in cancer cells. In this study, we examined whether Cal A could modulate TRAIL-induced apoptosis in human renal carcinoma-derived Caki cells. Our results show that Cal A is capable of sensitizing Caki cells to TRAIL-induced apoptosis, as well as U2OS human osteosarcoma cells and A549 human lung adenocarcinoma epithelial cells. Cal A increases intracellular ROS production and down-regulates c-FLIP(L) expression. Interestingly, the down-regulation of protein phosphatase 1 (PP1) by PP1 siRNA also reduced c-FLIP(L) expression via reactive oxygen species production. Furthermore, Cal A induced death receptor 4 (DR4) mRNA and protein expression by enhancing DR4 mRNA stability. We also found that PP4 siRNA up-regulated DR4 mRNA and protein expression. Collectively, our results suggest that Cal A could enhance TRAIL-mediated apoptosis via the down-regulation of c-FLIP(L) and the up-regulation of DR4 in human renal cell carcinoma cell line Caki.
机译：Calyculin A（Cal A）是一种丝氨酸/苏氨酸磷酸酶抑制剂，能够诱导癌细胞凋亡。在这项研究中，我们检查了Cal A是否可以调节TRAIL诱导的人肾癌衍生的Caki细胞凋亡。我们的结果表明，Cal A能够使Caki细胞对TRAIL诱导的细胞凋亡以及U2OS人骨肉瘤细胞和A549人肺腺癌上皮细胞敏感。 Cal A增加细胞内ROS的产生并下调c-FLIP（L）表达。有趣的是，PP1 siRNA对蛋白磷酸酶1（PP1）的下调也通过活性氧的产生降低了c-FLIP（L）的表达。此外，Cal A通过增强DR4 mRNA的稳定性诱导了死亡受体4（DR4）mRNA和蛋白表达。我们还发现PP4 siRNA上调DR4 mRNA和蛋白表达。总的来说，我们的结果表明，Cal A可以通过下调c-FLIP（L）和上调DR4在人肾癌细胞株Caki中的表达来增强TRAIL介导的细胞凋亡。

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