期刊
FASEB JOURNAL
卷 16, 期 12, 页码 1550-1557出版社
WILEY
DOI: 10.1096/fj.02-0541com
关键词
cancer; mitochondria; uncoupling proteins; membrane potential; oxygen consumption
资金
- NHLBI NIH HHS [R01 HL61346] Funding Source: Medline
- NIDDK NIH HHS [DK 56818] Funding Source: Medline
- NIGMS NIH HHS [R01 GM62562] Funding Source: Medline
Acquired or inherent drug resistance is the major problem in achieving successful cancer treatment. However, the mechanism(s) of pleiotropic drug resistance remains obscure. We have identified and characterized a cellular metabolic strategy that differentiates drug-resistant cells from drug-sensitive cells. This strategy may serve to protect drug-resistant cells from damage caused by chemotherapeutic agents and radiation. We show that drug-resistant cells have low mitochondrial membrane potential, use nonglucose carbon sources (fatty acids) for mitochondrial oxygen consumption when glucose becomes limited, and are protected from exogenous stress such as radiation. In addition, drug-resistant cells express high levels of mitochondrial uncoupling protein 2 (UCP2). The discovery of this metabolic strategy potentially facilitates the design of novel therapeutic approaches to drug resistance.
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