Targeting oxidative phosphorylation: why, when, and how
- PMID: 23518341
- DOI: 10.1016/j.ccr.2013.02.015
Targeting oxidative phosphorylation: why, when, and how
Abstract
In this issue of Cancer Cell, Vazquez and colleagues report reduced glycolysis and increased oxidative phosphorylation in certain melanomas, revealing metabolic plasticity rather than stable Warburg pathophysiology. Furthermore, Haq and colleagues (also in this issue of Cancer Cell) show situations where increased oxidative phosphorylation is required for melanomas to survive inhibition of B-RAF, suggesting investigation of therapeutic combinations of B-RAF inhibitors with biguanides.
Copyright © 2013 Elsevier Inc. All rights reserved.
Comment on
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PGC1α expression defines a subset of human melanoma tumors with increased mitochondrial capacity and resistance to oxidative stress.Cancer Cell. 2013 Mar 18;23(3):287-301. doi: 10.1016/j.ccr.2012.11.020. Epub 2013 Feb 14. Cancer Cell. 2013. PMID: 23416000 Free PMC article.
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Oncogenic BRAF regulates oxidative metabolism via PGC1α and MITF.Cancer Cell. 2013 Mar 18;23(3):302-15. doi: 10.1016/j.ccr.2013.02.003. Epub 2013 Mar 7. Cancer Cell. 2013. PMID: 23477830 Free PMC article.
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