In addition to their role in cellular homeostasis, pathways that regulate autophagy affect both tumorigenesis and tumor response to treatment. Therefore, understanding the regulation of autophagy in treated cancer cells is relevant to the discovery of molecular targets for the development of anti-cancer drugs. Our recent report points to radiation-induced inactivation of the mTOR pathway as an underlying mechanism of radiation-induced autophagy in the human breast cancer cell line MCF-7. Most importantly, radiation-induced inactivation of this pathway was detrimental to cell survival and was associated with reversal of mitochondrial ATPase activity and mitochondrial hyperpolarization, decreased level of eukaryotic initiation factor 4G (eIF4G) and increased phosphorylation of p53. Future analysis of the interrelationship among these events and the role each of them plays in cell survival following radiation will increase our ability to employ the mTOR pathway in anti-cancer therapy.

译文

除了它们在细胞内稳态中的作用外,调节自噬的途径还影响肿瘤发生和肿瘤对治疗的反应。因此,了解治疗癌细胞中自噬的调控与发现抗癌药物开发的分子靶标有关。我们最近的报告指出,辐射诱导的mTOR途径失活是辐射诱导的人乳腺癌细胞系MCF-7自噬的潜在机制。最重要的是,辐射诱导的该途径的失活对细胞存活有害,并且与线粒体ATPase活性和线粒体超极化的逆转,真核起始因子4G (eIF4G) 水平降低和p53磷酸化增加有关。对这些事件之间的相互关系以及它们在辐射后的细胞存活中所起的作用的未来分析将提高我们在抗癌治疗中采用mTOR途径的能力。

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