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自噬调节应激反应、代谢和抗癌免疫。

Autophagy Regulates Stress Responses, Metabolism, and Anticancer Immunity.

机构信息

Rutgers Cancer Institute of New Jersey, New Brunswick, NJ 08903, USA; Department of Molecular Biology and Biochemistry, Rutgers University, Piscataway, NJ 08854, USA; Ludwig Princeton Branch, Ludwig Institute for Cancer Research, Princeton University, Princeton, NJ, USA.

Rutgers Cancer Institute of New Jersey, New Brunswick, NJ 08903, USA; Department of Surgery, Robert Wood Johnson Medical School, Rutgers University, New Brunswick, NJ, USA.

出版信息

Trends Cancer. 2021 Aug;7(8):778-789. doi: 10.1016/j.trecan.2021.05.003. Epub 2021 Jun 7.

Abstract

Autophagy is a catabolic intracellular nutrient-scavenging pathway triggered by nutrient deprivation and stress that captures and degrades intracellular proteins and organelles in lysosomes. The breakdown products are then recycled into metabolic pathways to sustain survival. Organelle turnover by autophagy contributes to quality control and suppresses inflammation. Autophagy is upregulated in many cancers and supports their growth, survival, and malignancy in a tumor cell-autonomous fashion. Host autophagy also promotes tumor growth by maintaining a supply of essential nutrients and suppressing innate and adaptive antitumor immune responses. Autophagy is also upregulated in response to cancer therapy and confers treatment resistance. Thus, autophagy is a cancer vulnerability and its inhibition is under investigation as a novel therapeutic approach.

摘要

自噬是一种由营养缺乏和应激触发的分解代谢性细胞内营养物质回收途径,它可以在溶酶体中捕获和降解细胞内蛋白质和细胞器。然后,这些分解产物被回收再利用到代谢途径中,以维持生存。自噬的细胞器周转率有助于质量控制并抑制炎症。自噬在许多癌症中上调,并以肿瘤细胞自主的方式支持其生长、存活和恶性转化。宿主自噬还通过维持必需营养物质的供应和抑制先天和适应性抗肿瘤免疫反应来促进肿瘤生长。自噬也会对癌症治疗产生反应,并导致治疗耐药性。因此,自噬是一种癌症弱点,抑制自噬作为一种新的治疗方法正在研究中。

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