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首页> 美国卫生研究院文献>International Journal of Molecular Sciences >Inhibition of Autophagy Potentiates Atorvastatin-Induced Apoptotic Cell Death in Human Bladder Cancer Cells in Vitro
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Inhibition of Autophagy Potentiates Atorvastatin-Induced Apoptotic Cell Death in Human Bladder Cancer Cells in Vitro

机译：自噬的抑制作用增强了阿托伐他汀诱导的人膀胱癌细胞的凋亡。

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Statins are cholesterol reduction agents that exhibit anti-cancer activity in several human cancers. Because autophagy is a crucial survival mechanism for cancer cells under stress conditions, cooperative inhibition of autophagy acts synergistically with other anti-cancer drugs. Thus, this study investigates whether combined treatment of atorvastatin and autophagy inhibitors results in enhancing the cytotoxic effects of atorvastatin, upon human bladder cancer cells, T24 and J82, in vitro. To measure cell viability, we performed the EZ-Cytox cell viability assay. We examined apoptosis by flow cytometry using annexin-V/propidium iodide (PI and western blot using procaspase-3 and poly (ADP-ribose) polymerase (PARP) antibodies. To examine autophagy activation, we evaluated the co-localization of LC3 and LysoTracker by immunocytochemistry, as well as the expression of LC3 and p62/sequestosome-1 (SQSTM1) by western blot. In addition, we assessed the survival and proliferation of T24 and J82 cells by a clonogenic assay. We found that atorvastatin reduced the cell viability of T24 and J82 cells via apoptotic cell death and induced autophagy activation, shown by the co-localization of LC3 and LysoTracker. Moreover, pharmacologic inhibition of autophagy significantly enhanced atorvastatin-induced apoptosis in T24 and J82 cells. In sum, inhibition of autophagy potentiates atorvastatin-induced apoptotic cell death in human bladder cancer cells in vitro, providing a potential therapeutic approach to treat bladder cancer.
机译：他汀类药物是胆固醇降低剂，在几种人类癌症中均表现出抗癌活性。由于自噬是应激条件下癌细胞的重要生存机制，因此自噬的协同抑制作用与其他抗癌药物协同作用。因此，本研究调查了阿托伐他汀和自噬抑制剂的联合治疗是否在体外增强了阿托伐他汀对人膀胱癌细胞T24和J82的细胞毒性作用。为了测量细胞活力，我们进行了EZ-Cytox细胞活力测定。我们使用Annexin-V /碘化丙啶通过流式细胞术检查了细胞凋亡（PI和使用procaspase-3和聚（ADP-核糖）聚合酶（PARP）抗体的Western印迹法。为了检查自噬激活，我们评估了LC3和LysoTracker的共定位免疫细胞化学法检测LC3和p62 / sequestosome-1（SQSTM1）的表达，并用克隆法检测T24和J82细胞的存活和增殖，发现阿托伐他汀降低了细胞活力LC3和LysoTracker的共定位表明，通过凋亡引起的T24和J82细胞凋亡和诱导的自噬激活，此外，自噬的药理学抑制作用显着增强了阿托伐他汀诱导的T24和J82细胞的凋亡。阿托伐他汀在体外诱导人膀胱癌细胞凋亡，为膀胱癌的治疗提供了可能。

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