Journal
CURRENT OPINION IN GENETICS & DEVELOPMENT
Volume 20, Issue 1, Pages 51-56Publisher
CURRENT BIOLOGY LTD
DOI: 10.1016/j.gde.2009.10.009
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Funding
- National Cancer Institute
- National Heart, Lung, and Blood Institute
- National Institute of General Medical Sciences
- Johns Hopkins Institute for Cell Engineering
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Hypoxia-inducible factor 1 (HIF-1) plays a key role in the reprogramming of cancer metabolism by activating transcription of genes encoding glucose transporters and glycolytic enzymes, which take up glucose and convert it to lactate; pyruvate dehydrogenase kinase 1, which shunts pyruvate away from the mitochondria; and BNIP3, which triggers selective mitochondrial autophagy. The shift from oxidative to glycolytic metabolism allows maintenance of redox homeostasis and cell survival under conditions of prolonged hypoxia. Many metabolic abnormalities in cancer cells increase HIF-1 activity. As a result, a feed-forward mechanism can be activated that drives HIF-1 activation and may promote tumor progression.
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