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首页> 外文期刊>Journal of cellular physiology. >Caveolin-1 knockdown increases the therapeutic sensitivity of lung cancer to cisplatin-induced apoptosis by repressing Parkin-related mitophagy and activating the ROCK1 pathway
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Caveolin-1 knockdown increases the therapeutic sensitivity of lung cancer to cisplatin-induced apoptosis by repressing Parkin-related mitophagy and activating the ROCK1 pathway

机译：Caveolin-1击倒增加了治疗cisplatin-induced敏感性的肺癌细胞凋亡的抑制Parkin-related mitophagyROCK1途径激活

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Chemotherapy is the first-line treatment option for patients with lung cancer. However, therapeutic resistance occurs through an incompletely understood mechanism. Our research wants to investigate the influence of Caveolin-1 (Cav-1) on the therapeutic sensitivity of lung cancer in vitro. Results in this study demonstrated that Cav-1 levels were markedly inhibited in A549 lung cancer cells after exposure to cisplatin. Knockdown of caveolin further enhanced cisplatin-triggered cancer death in A549 cells. The functional investigation demonstrated that Cav-1 inhibition amplified the mitochondrial stress signaling induced by cisplatin, as evidenced by the mitochondrial reactive oxygen species burst, cellular metabolic disruption, mitochondrial membrane potential reduction, and mitochondrial caspase-9-related apoptosis activation. At the molecular level, cav-1 augmented cisplatin-mediated mitochondrial damage by inhibiting Parkin-related mitochondrial autophagy. Mitophagy activation effectively attenuated the promotive impact of Cav-1 knockdown on mitochondrial damage and cell death. Furthermore, our data indicated that Cav-1 affected Parkin-related mitophagy by activating the Rho-associated coiled-coil kinase 1 (ROCK1) pathway; inhibition of the ROCK1 axis prevented cav-1 knockdown-mediated cell death and mitochondrial damage. Taken together, our results provide ample data illuminate the necessary action exerted by Cav-1 on affecting cisplatin-related therapeutic resistance. Silencing of Cav-1 inhibited Parkin-related mitophagy, thus amplifying cisplatin-mediated mitochondrial apoptotic signaling. This finding identifies the Cav-1/ROCK1/Parkin/mitophagy axis as a potential target to overcome cisplatin-related resistance in lung cancer cells.
机译：化疗是一线治疗的选择肺癌患者。治疗耐药性发生通过不完全理解机制。想调查Caveolin-1的影响肺(Cav-1)治疗的敏感性癌症在体外。证明Cav-1显著水平抑制A549肺癌细胞顺铂。进一步加强cisplatin-triggered癌症死亡在A549细胞。证明Cav-1抑制放大线粒体应激引起的信号由线粒体顺铂,就是明证活性氧破裂,细胞代谢中断,线粒体膜电位减少,线粒体caspase-9-related细胞凋亡激活。cav-1增强cisplatin-mediated线粒体通过抑制Parkin-related线粒体损害自噬。减毒Cav-1的奖励的影响可拆卸的线粒体损伤和细胞死亡。此外,我们的数据表明Cav-1影响Parkin-related mitophagy通过激活的Rho-associated卷曲螺旋激酶1 (ROCK1)通路;cav-1 knockdown-mediated细胞死亡线粒体损伤。提供充足的数据说明的必要行动Cav-1施加的影响cisplatin-related治疗抵抗。Cav-1抑制Parkin-related沉默mitophagy,从而放大cisplatin-mediated线粒体凋亡信号。标识Cav-1 / ROCK1 /帕金/ mitophagy轴作为一个潜在的目标来克服在肺癌cisplatin-related抵抗细胞。

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