The dual role of autophagy in cancer
The dual role of autophagy in cancer
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DOI：
10.1016/j.coph.2011.03.009
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发表时间：
2011-08-01
影响因子：
4
通讯作者：
Eskelinen, Eeva-Liisa
中科院分区：
文献类型：
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作者：
Eskelinen, Eeva-Liisa
自噬是细胞质物质、受损细胞器和溶酶体中易于聚集的蛋白质的降解机制。最近的证据表明，自噬是一种肿瘤抑制机制，这与其在清除支架蛋白p62/SQSTM 1和预防氧化应激和基因组不稳定性中的作用有关。然而，由于自噬是一种生存机制，癌细胞也可以利用它来生存营养限制和缺氧，经常发生在实体瘤。肿瘤细胞也可以上调自噬作为对癌症治疗的反应，最近的研究表明，抑制自噬可以增强治疗后对肿瘤细胞的杀伤。有趣的是，FK 506结合蛋白51在恶性黑色素瘤的自噬相关辐射抗性中发挥作用。
Autophagy is a mechanism for the degradation of cytoplasmic material, damaged organelles and aggregate-prone proteins in lysosomes. Recent evidence indicates that autophagy is a tumor suppressor mechanism, which is connected to its role in the clearance of the scaffold protein p62/SQSTM1 and prevention of oxidative stress and genomic instability. However, since autophagy is a survival mechanism, cancer cells can also exploit it to survive nutrient limitation and hypoxia that often occur in solid tumors. Tumor cells can also upregulate autophagy as a response to cancer treatment, and recent studies show that inhibition of autophagy can enhance the killing of tumor cells after treatment. Interestingly, the FK506-binding protein 51 plays a role in the autophagy-linked radiation resistance of malignant melanoma.