Abstract
In this issue of Cancer Cell, Finley and coworkers report that the genetic loss of the deacetylase SIRT3 leads to metabolic reprogramming toward glycolysis. This shift is mediated by an increase in cellular reactive oxygen species (ROS) generation that amplifies HIF-α stabilization and HIF-dependent gene expression, thereby driving the tumor phenotype.
Copyright © 2011 Elsevier Inc. All rights reserved.
MeSH terms
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Animals
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Cell Line, Tumor
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Cells, Cultured
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Fibroblasts / cytology
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Fibroblasts / metabolism
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Glucose / metabolism
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Glycolysis
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Humans
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Hypoxia-Inducible Factor 1, alpha Subunit / metabolism*
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Metabolomics / methods
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Mice
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Mice, Knockout
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Models, Biological
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Neoplasms / genetics
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Neoplasms / metabolism*
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Neoplasms / pathology
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Reactive Oxygen Species / metabolism*
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Sirtuin 3 / genetics
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Sirtuin 3 / metabolism*
Substances
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Hypoxia-Inducible Factor 1, alpha Subunit
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Reactive Oxygen Species
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SIRT3 protein, human
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Sirtuin 3
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Glucose