Abstract
Abstract p53 is a key player in the cellular stress response. Apart from its canonical role in cell checkpoint functions, p53 also regulates cellular metabolism by blocking glycolysis and promoting oxidative phosphorylation. The hypoxia-inducible factor 1(HIF-1), on the other hand, is a master transcription factor promoting glycolysis. We describe a previously unrecognized metabolic response to low levels of stress, including low doses of ionizing radiation or arsenic. By using an integrated approach, we demonstrate that low-level stress induces a metabolic shift from oxidative phosphorylation to aerobic glycolysis leading to increased stress tolerance in both cell and animal models. Low-level stress-induced metabolic changes are mediated by a functional cooperation between p53 and HIF-1α. Our work provides a novel metabolic mechanism of the stress response. Citation Format: Suthakar Ganapathy, Zhi-Min Yuan. A p53/HIF-1alpha-mediated metabolic response to stress. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 4335. doi:10.1158/1538-7445.AM2014-4335
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