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

:除了在细胞稳态中的作用外,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,了解在治疗的癌细胞中自噬的调控与发现抗癌药物的分子靶标有关。我们最近的报告指出,辐射诱导的mTOR途径失活是人类乳腺癌细胞系MCF-7辐射诱导的自噬的潜在机制。最重要的是,此途径的辐射诱导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)的水平降低以及p53磷酸化的增加有关。进一步分析这些事件之间的相互关系以及它们各自在放射后的细胞存活中所起的作用,将提高我们在抗癌治疗中采用mTOR途径的能力。

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