4.5 Article

Role of autophagy in suppression of inflammation and cancer

期刊

CURRENT OPINION IN CELL BIOLOGY
卷 22, 期 2, 页码 212-217

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CURRENT BIOLOGY LTD
DOI: 10.1016/j.ceb.2009.12.008

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资金

  1. National Institutes of Health
  2. National Cancer Institute [R37 CA53370, RO1 CA130893, RO1 CA147961]
  3. Department of Defense [DODW81XWH-09-01-0394]
  4. New Jersey Commission for Cancer Research [09-1083-CCR-EO, 09-2406-CCR-EO]
  5. Pharmaceutical Industry
  6. NATIONAL CANCER INSTITUTE [R37CA053370, R01CA163591, RC1CA147961, R01CA130893] Funding Source: NIH RePORTER

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Autophagy is a crucial component of the cellular stress adaptation response that maintains mammalian homeostasis. Autophagy protects against neurodegenerative and inflammatory conditions, aging, and cancer. This is accomplished by the degradation and intracellular recycling of cellular components to maintain energy metabolism and by damage mitigation through the elimination of damaged proteins and organelles. How autophagy modulates oncogenesis is gradually emerging. Tumor cells induce autophagy in response to metabolic stress to promote survival, suggesting deployment of therapeutic strategies to block autophagy for cancer therapy. By contrast, defects in autophagy lead to cell death, chronic inflammation, and genetic instability. Thus, stimulating autophagy may be a powerful approach for chemoprevention. Analogous to infection or toxins that create persistent tissue damage and chronic inflammation that increases the incidence of cancer, defective autophagy represents a cell-intrinsic mechanism to create the damaging, inflammatory environment that predisposes to cancer. Thus, cellular damage mitigation through autophagy is a novel mechanism of tumor suppression.

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