Chaperone-mediated autophagy substrate proteins in cancer.

Chaperone-mediated autophagy substrate proteins in cancer.
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DOI:
10.18632/oncotarget.17583
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发表时间:
2017-08-01
期刊:
影响因子:
--
通讯作者:
Zhou DH
Zhou DH
中科院分区:
其他
文献类型:
--
作者:
Tang Y;Wang XW;Liu ZH;Sun YM;Tang YX;Zhou DH

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所有细胞内蛋白质都经历连续的合成和降解。分子伴侣介导的自噬(CMA)是通过胞质蛋白(底物蛋白)的周转来维持细胞稳态所必需的。这种降解涉及一系列底物蛋白,包括癌症启动子和抑制子。由于激活或抑制CMA通路来治疗癌症仍然存在争议,靶向CMA底物蛋白提供了一个新的方向。本文综述了CMA降解的肿瘤相关底物蛋白。因此,CMA底物蛋白催化糖酵解,这有助于癌细胞中的瓦尔堡效应。基于CMA的底物蛋白的降解可以通过翻译后修饰如磷酸化或乙酰化来改变。总之,靶向CMA底物蛋白发展成为一种新的抗癌治疗方法。
All intracellular proteins undergo continuous synthesis and degradation. Chaperone-mediated autophagy (CMA) is necessary to maintain cellular homeostasis through turnover of cytosolic proteins (substrate proteins). This degradation involves a series of substrate proteins including both cancer promoters and suppressors. Since activating or inhibiting CMA pathway to treat cancer is still debated, targeting to the CMA substrate proteins provides a novel direction. We summarize the cancer-associated substrate proteins which are degraded by CMA. Consequently, CMA substrate proteins catalyze the glycolysis which contributes to the Warburg effect in cancer cells. The fact that the degradation of substrate proteins based on the CMA can be altered by posttranslational modifications such as phosphorylation or acetylation. In conclusion, targeting to CMA substrate proteins develops into a new anticancer therapeutic approach.
DOI: 10.1016/s0360-3016(01)01630-3
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