Cancer's sweet tooth.
Even in the presence of an adequate oxygen supply, many tumors metabolize the majority of the glucose they take up through glycolysis. It has been a long-held belief that this glycolytic phenotype is due to cancer-specific defects in mitochondrial oxidative phosphorylation. In this issue of Cancer Cell, Fantin et al. now report that most tumor cells have a substantial reserve capacity to produce ATP by oxidative phosphorylation when glycolysis is suppressed. These new data add to mounting evidence that the high rate of glycolysis exhibited by most tumors is required to support cell growth rather than to compensate for defect(s) in mitochondrial function.
Bui
Thi
T
The Abramson Family Cancer Research Institute and the Department of Medicine, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104, USA.
Thompson
Craig B
CB
D000255:Adenosine Triphosphate / Q000096:biosynthesis; D000818:Animals; D002471:Cell Transformation, Neoplastic / Q000378:metabolism* / Q000473:pathology; D004734:Energy Metabolism; D005947:Glucose / Q000378:metabolism*; D006019:Glycolysis; D006801:Humans; D051795:Hypoxia-Inducible Factor 1, alpha Subunit / Q000096:biosynthesis; D008928:Mitochondria / Q000378:metabolism / Q000502:physiology; D009369:Neoplasms / Q000378:metabolism* / Q000473:pathology; D010085:Oxidative Phosphorylation; D010101:Oxygen Consumption
C497442:HIF1A protein, human; D051795:Hypoxia-Inducible Factor 1, alpha Subunit; D000255:Adenosine Triphosphate; D005947:Glucose