Journal
FASEB JOURNAL
Volume 16, Issue 12, Pages 1550-1557Publisher
WILEY
DOI: 10.1096/fj.02-0541com
Keywords
cancer; mitochondria; uncoupling proteins; membrane potential; oxygen consumption
Categories
Funding
- NHLBI NIH HHS [R01 HL61346] Funding Source: Medline
- NIDDK NIH HHS [DK 56818] Funding Source: Medline
- NIGMS NIH HHS [R01 GM62562] Funding Source: Medline
Ask authors/readers for more resources
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.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available