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一种由 PINK1 介导的线粒体自噬通路决定了肿瘤的命运——是良性还是恶性?

A PINK1-mediated mitophagy pathway decides the fate of tumors-to be benign or malignant?

机构信息

a Department of Pharmacology, Toxicology and Therapeutics , University of Kansas Medical Center , Kansas City , KS , USA.

出版信息

Autophagy. 2018;14(4):563-566. doi: 10.1080/15548627.2018.1425057. Epub 2018 Feb 21.

Abstract

Macroautophagy/autophagy plays a dual role in cancer depending on the stage of tumorigenesis. Autophagy prevents tumor initiation by suppressing chronic tissue damage, inflammation, accumulation of damaged organelles and genome instability. Autophagy can also sustain tumor metabolism and provide nutrients for tumor growth and survival via nutrient recycling. Moreover, autophagy is required for benign tumors to progress to malignant tumors. Emerging evidence indicates that autophagy or mitophagy can inactivate tumor suppressors such as TP53/TRP53/p53 to promote tumor progression once carcinogenesis has been initiated.

摘要

自噬/巨自噬在癌症中具有双重作用,取决于肿瘤发生的阶段。自噬通过抑制慢性组织损伤、炎症、受损细胞器的积累和基因组不稳定性来防止肿瘤的起始。自噬还可以通过营养物质的再循环来维持肿瘤代谢,并为肿瘤的生长和存活提供营养物质。此外,自噬对于良性肿瘤向恶性肿瘤的进展是必需的。新出现的证据表明,一旦致癌作用被引发,自噬或线粒体自噬可以使肿瘤抑制因子如 TP53/TRP53/p53 失活,从而促进肿瘤的进展。

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本文引用的文献

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PINK1 is degraded through the N-end rule pathway.PINK1 通过 N 端规则途径降解。
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