Journal
BRITISH JOURNAL OF CANCER
Volume 105, Issue 4, Pages 469-474Publisher
SPRINGERNATURE
DOI: 10.1038/bjc.2011.245
Keywords
uncoupling proteins; UCP2; aerobic glycolysis; metabolic reprogramming; oxidative stress; p53
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Funding
- NHLBI NIH HHS [R01 HL094400, R01 HL094400-01] Funding Source: Medline
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Recent findings link metabolic transformation of cancer cells to aberrant functions of mitochondrial uncoupling proteins (UCPs). By inducing proton leak, UCPs interfere with mitochondrial synthesis of adenosine 5'-triphosphate, which is also a key determinant of glycolytic pathways. In addition, UCP suppress the generation of superoxide, a byproduct of mitochondrial electron transport and a major source of oxidative stress. The near ubiquitous UCP2 becomes highly abundant in some cancers and may advance metabolic reprogramming, further disrupt tumour suppression, and promote chemoresistance. Here we review current evidence to suggest that inhibition of mitochondrial uncoupling may eliminate these responses and reveal novel anti-cancer strategies. British Journal of Cancer (2011) 105, 469-474. doi: 10.1038/bjc. 2011.245 www.bjcancer.com Published online 28 June 2011 (C) 2011 Cancer Research UK
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