SIRT1 and p53, effect on cancer, senescence and beyond

• Published in: Biochimica et biophysica acta Vol. 1804; no. 8; pp. 1684 - 1689
• Main Authors: Yi, Jingjie, Luo, Jianyuan
• Format: Journal Article
• Language: English
• Published: Netherlands Elsevier B.V 01.08.2010
• Subjects: Acetylation; Aging - metabolism; Animals; Apoptosis; Cancer; Cellular Senescence; Deacetylation; Humans; Mice; Models, Biological; Neoplasms - etiology; Neoplasms - metabolism; Nerve Degeneration - etiology; Nerve Degeneration - metabolism; Oxidative Stress; p53; Senescence; Signal Transduction; SIRT1; Sirtuin 1 - metabolism; Tumor Suppressor Protein p53 - metabolism; Senescence; Acetylation; Deacetylation; SIRT1; p53; Cancer
• ISSN: 1570-9639; 0006-3002; 1878-1454
• DOI: 10.1016/j.bbapap.2010.05.002

NAD +-dependent Class III histone deacetylase SIRT1 is a multiple function protein critically involved in stress responses, cellular metabolism and aging through deacetylating a variety of substrates including p53, forkhead-box transcription factors, PGC-1α, NF-κB, Ku70 and histones. The first discovered non-histone target of SIRT1, p53, is suggested to play a central role in SIRT1-mediated functions in tumorigenesis and senescence. SIRT1 was originally considered to be a potential tumor promoter since it negatively regulates the tumor suppressor p53 and other tumor suppressors. There is new evidence that SIRT1 acts as a tumor suppressor based on its role in negatively regulating β-catenin and survivin. This review provides an overview of current knowledge of SIRT1-p53 signaling and controversies regarding the functions of SIRT1 in tumorigenesis.