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首页> 外文期刊>Journal of cellular physiology. >AMPK-mTOR-ULK1 axis activation-dependent autophagy promotes hydroxycamptothecin-induced apoptosis in human bladder cancer cells
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AMPK-mTOR-ULK1 axis activation-dependent autophagy promotes hydroxycamptothecin-induced apoptosis in human bladder cancer cells

机译：AMPK-mTOR-ULK1轴activation-dependent自噬促进hydroxycamptothecin-induced细胞凋亡在人类膀胱癌细胞

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摘要

10-hydroxycamptothecin (HCPT), a natural plant extract, exerts anticancer capacity. HCPT has been reported to induce apoptosis and autophagy in human cancer cells. The interaction between autophagy and apoptosis induced by HCPT and the molecular mechanism in bladder cancer cells were investigated in this study. Our results confirmed that HCPT suppressed cell viability and migration and caused cell-cycle arrest in T24 and 5637. Then, we used Z-VAD(OMe)-FMK to clarify that apoptosis induced by HCPT was mediated by caspase. Moreover, HCPT boosted autophagy through activating the AMPK/mTOR/ULK1 pathway. Blocking autophagy by 3-methyladenine, the adenosine monophosphate-activated protein kinase (AMPK) inhibitor dorsomorphin and siATG7 reversed HCPT-induced cytotoxicity. Conversely, rapamycin and the AMPK activator AICAR enhanced growth inhibition and cell apoptosis, suggesting that autophagy played a proapoptosis role. Taken together, our findings showed that HCPT-induced autophagy mediated by the AMPK pathway in T24 and 5637 cell lines, which reinforced the apoptosis, indicating that HCPT together with autophagy activator would be a novel strategy for clinical treatment in bladder cancer.
机译：10-hydroxycamptothecin(羟基喜树碱),天然植物提取、发挥抗癌能力。据报道,诱导细胞凋亡和自噬在人类癌症细胞。自噬和羟基喜树碱诱导细胞凋亡在膀胱癌细胞分子机制在这项研究调查。羟基喜树碱抑制细胞生存能力和迁移导致T24细胞循环逮捕和5637。然后,我们使用Z-VAD(当地)-FMK澄清羟基喜树碱诱导细胞凋亡介导半胱天冬酶。激活AMPK / mTOR / ULK1通路。自噬通过3-methyladenine,腺苷monophosphate-activated蛋白激酶(AMPK)抑制剂dorsomorphin和siATG7逆转HCPT-induced细胞毒性。的AMPK激活爱卡增强经济增长抑制和细胞凋亡,表明自噬发挥了proapoptosis作用。在一起,我们的研究结果表明,HCPT-induced自噬的T24, AMPK途径5637细胞系,强化细胞凋亡,表明羟基喜树碱与自噬催化剂将是一个临床的新策略治疗膀胱癌。

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