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Autophagy is a therapeutic target in anticancer drug resistance.

机译:自噬是抗癌药物耐药性的治疗目标。

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摘要

Autophagy is a type of cellular catabolic degradation response to nutrient starvation or metabolic stress. The main function of autophagy is to maintain intracellular metabolic homeostasis through degradation of unfolded or aggregated proteins and organelles. Although autophagic regulation is a complicated process, solid evidence demonstrates that the PI3K-Akt-mTOR, LKB1-AMPK-mTOR and p53 are the main upstream regulators of the autophagic pathway. Currently, there is a bulk of data indicating the important function of autophagy in cancer. It is noteworthy that autophagy facilitates the cancer cells' resistance to chemotherapy and radiation treatment. The abrogation of autophagy potentiates the re-sensitization of therapeutic resistant cancer cells to the anticancer treatment via autophagy inhibitors, such as 3-MA, CQ and BA, or knockdown of the autophagy related molecules. In this review, we summarize the accumulation of evidence for autophagy's involvement in mediating resistance of cancer cells to anticancer therapy and suggest that autophagy might be a potential therapeutic target in anticancer drug resistance in the future.
机译:自噬是细胞对营养缺乏或代谢应激的分解代谢降解反应的一种。自噬的主要功能是通过降解未折叠或聚集的蛋白质和细胞器来维持细胞内代谢稳态。尽管自噬调节是一个复杂的过程,但有确凿的证据表明PI3K-Akt-mTOR,LKB1-AMPK-mTOR和p53是自噬通路的主要上游调节剂。当前,有大量数据表明自噬在癌症中的重要作用。值得注意的是,自噬促进了癌细胞对化学疗法和放射治疗的抵抗力。自噬的废除通过自噬抑制剂(例如3-MA,CQ和BA)或敲低自噬相关分子,增强了治疗性耐药性癌细胞对抗癌治疗的再敏感性。在这篇综述中,我们总结了自噬参与介导癌细胞对抗癌治疗的耐药性的证据积累,并提出自噬可能成为将来抗癌药物耐药性的潜在治疗靶标。

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