期刊
JOURNAL OF CLINICAL INVESTIGATION
卷 125, 期 1, 页码 42-46出版社
AMER SOC CLINICAL INVESTIGATION INC
DOI: 10.1172/JCI73941
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资金
- NIH [R01CA163591, R01CA130893]
- Val Skinner Foundation
- New Jersey Commission for Cancer Research
- Rutgers Cancer Institute of New Jersey
- NATIONAL CANCER INSTITUTE [RC1CA147961, R01CA053370, R37CA053370, R01CA130893, R01CA163591] Funding Source: NIH RePORTER
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.
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