Journal
BIOCHEMICAL PHARMACOLOGY
Volume 92, Issue 1, Pages 149-156Publisher
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.bcp.2014.08.034
Keywords
p53; SIRT1; Metabolism; Tumor suppression; Genome integrity
Categories
Funding
- AIRC (Italian Association for Cancer Research, IG grant) [11344]
- Recherche Cancer et Sang
- Recherches Scientifiques Luxembourg association
- Een Haerz fir kriibskrank Kanner association
- Action Lions Vaincre le Cancer association
- Televie Luxembourg
- National Research Foundation of Korea (NRF) grant - Korea Government, Ministry of Science, ICT & Future Planning (MSIP) [2011-0030001]
- National Research Foundation of Korea [2011-0030001] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
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The tumor suppressor p53 is a transcription factor that regulates key processes. But, the outcomes of the p53 response go beyond its role as a nuclear transcription factor. Sirtuin (SIRT1) regulates p53 functions as transcription factor. At the same time, SIRT1 protects the genome under stress conditions. The link between p53 and SIRT1 responses is unique. Both regulate metabolism, stress signaling, cell survival, cell cycle control and genome stability. Recent studies have proposed cancer as a metabolic disease. This is due to the switch from aerobic to anaerobic metabolism during tumor development. Yet, the complex molecular circuits (in and out of the nucleus) of tumor progression remain elusive. In this review, we will focus on the interplay between p53 and SIRT1. We will discuss their roles as nodes for possible therapeutic intervention. (C) 2014 Elsevier Inc. All rights reserved.
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