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Regulation of cellular senescence by p53

Authors


J. Campisi, Life Sciences Division, Lawrence Berkeley National Laboratory, Mailstop 84-171, 1 Cyclotron Road, Berkeley, CA 94720, USA. Fax: + 1 510 486 4545, Tel.: + 1 510 486 4416, E-mail: jcampisi@lbl.gov

Abstract

Many normal cells respond to potentially oncogenic stimuli by undergoing cellular senescence, a state of irreversibly arrested proliferation and altered differentiated function. Cellular senescence very likely evolved to suppress tumorigenesis. In support of this idea, it is regulated by several tumor suppressor genes. At the heart of this regulation is p53. p53 is essential for the senescence response to short telomeres, DNA damage, oncogenes and supraphysiological mitogenic signals, and overexpression of certain tumor suppressor genes. Despite the well-documented central role for p53 in the senescence response, many questions remain regarding how p53 senses senescence-inducing stimuli and how it elicits the senescent phenotype.

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