机构:
Univ Med & Dent New Jersey, Robert Wood Johnson Med Sch, Dept Pharmacol, Piscataway, NJ 08854 USAUniv Med & Dent New Jersey, Robert Wood Johnson Med Sch, Dept Pharmacol, Piscataway, NJ 08854 USA
Jin, SK
[1
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机构:
[1] Univ Med & Dent New Jersey, Robert Wood Johnson Med Sch, Dept Pharmacol, Piscataway, NJ 08854 USA
[2] Univ Med & Dent New Jersey, Robert Wood Johnson Med Sch, Canc Inst New Jersey, Piscataway, NJ 08854 USA
Autophagy was recently established as a novel tumor suppression mechanism, which stimulated a wave of investigations that were aimed at understanding exactly how autophagy prevents tumorigenesis, as well as to determine to what extent autophogy is implicated in human cancers. Autophagy might exert its tumor suppression function at the subcellular level by removing defective cytoplasmic components, such as damaged mitochondria. In addition, it might function at the cellular level by helping in the orderly removal of damaged cells. Previous studies indicated that autophagy is compromised in human breast, ovarian and prostate cancers. Recent research revealed that autophogy is activated by p53, a critical tumor suppressor that is involved in most, if not all, tumorigenesis. This study places autophagy in a broader context of human cancers. Future work elucidating the role of autophagy in the p53 circuit and p53 function might provide more insight into tumorigenesis and targeted cancer chemotherapy.
机构:
Univ Colorado, Howard Hughes Med Inst, Boulder, CO 80309 USA
Univ Colorado, Dept Mol Cellular & Dev Biol, Boulder, CO 80309 USAUniv Colorado, Howard Hughes Med Inst, Boulder, CO 80309 USA
Mellert, Hestia
Espinosa, Joaquin M.
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机构:
Univ Colorado, Howard Hughes Med Inst, Boulder, CO 80309 USA
Univ Colorado, Dept Mol Cellular & Dev Biol, Boulder, CO 80309 USAUniv Colorado, Howard Hughes Med Inst, Boulder, CO 80309 USA