The role for autophagy in cancer

被引:1434
作者
White, Eileen [1 ,2 ]
机构
[1] Rutgers Canc Inst New Jersey, New Brunswick, NJ 08903 USA
[2] Rutgers State Univ, Dept Mol Biol & Biochem, Piscataway, NJ 08855 USA
关键词
STRESS-INDUCED AUTOPHAGY; TUMORIGENESIS; GENE; P62; PROGRESSION; BECLIN-1; TUMORS; INFLAMMATION; METABOLISM; GROWTH;
D O I
10.1172/JCI73941
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
100103 [病原生物学]; 100218 [急诊医学];
摘要
Autophagy is a survival-promoting pathway that captures, degrades, and recycles intracellular proteins and organelles in lysosomes. Autophagy preserves organelle function, prevents the toxic buildup of cellular waste products, and provides substrates to sustain metabolism in starvation. Although in some contexts autophagy suppresses tumorigenesis, in most contexts autophagy facilitates tumorigenesis. Cancers can upregulate autophagy to survive microenvironmental stress and to increase growth and aggressiveness. Mechanisms by which autophagy promotes cancer include suppressing induction of the p53 tumor suppressor protein and maintaining metabolic function of mitochondria. Efforts to inhibit autophagy to improve cancer therapy have thereby attracted great interest.
引用
收藏
页码:42 / 46
页数:5
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