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SIRT3 controls cancer metabolic reprogramming by regulating ROS and HIF
1Department of Pediatrics, Northwestern University Feinberg School of Medicine, 310 E. Superior St. Searle Bldg. 4-685, Chicago, IL 60611, USA. p-schumacker@northwestern.edu
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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.
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