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.
Original language | English (US) |
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Pages (from-to) | 299-300 |
Number of pages | 2 |
Journal | Cancer Cell |
Volume | 19 |
Issue number | 3 |
DOIs | |
State | Published - Mar 8 2011 |
ASJC Scopus subject areas
- Oncology
- Cell Biology
- Cancer Research