期刊
ACS CHEMICAL BIOLOGY
卷 14, 期 11, 页码 2335-2348出版社
AMER CHEMICAL SOC
DOI: 10.1021/acschembio.9b00338
关键词
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资金
- National Institutes of Health [R01-CA120439]
- National Institutes of Health Chemistry-Biology Interface Training Program [T32-GM070421]
Many anticancer strategies rely on the promotion of apoptosis in cancer cells as a means to shrink tumors. Crucial for apoptotic function are executioner caspases, most notably caspase-3, that proteolyze a variety of proteins, inducing cell death. Paradoxically, overexpression of procaspase-3 (PC-3), the low-activity zymogen precursor to caspase-3, has been reported in a variety of cancer types. Until recently, this counterintuitive overexpression of a pro-apoptotic protein in cancer has been puzzling. Recent studies suggest subapoptotic caspase-3 activity may promote oncogenic transformation, a possible explanation for the enigmatic overexpression of PC-3. Herein, the overexpression of PC-3 in cancer and its mechanistic basis is reviewed; collectively, the data suggest the potential for exploitation of PC-3 overexpression with PC-3 activators as a targeted anticancer strategy.
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