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Senescence

The more the merrier

Nature Reviews Cancer volume 9, pages 688–689 (2009)Cite this article

TP53, the human gene that encodes p53, contains an alternative promoter and produces multiple splice variants, which are known as the p53 isoforms. To investigate the roles of two human p53 isoforms — p53β (which lacks the carboxy-terminal oligomerization domain) and Δ133p53 (which lacks the amino-terminal transactivation and proline-rich domains) — Fujita et al. examined their expression profiles during senescence both in vitro and in vivo.

Replicatively senescent normal human diploid fibroblasts showed increased expression of p53β but decreased expression of Δ133p53. To determine the functional significance of this senescence-associated p53 isoform expression pattern, a series of knockdown and overexpression experiments were carried out. Both retroviral p53β overexpression and RNA interference-mediated knock down of Δ133p53 were able to induce p53-dependent cellular senescence. Conversely, Δ133p53 overexpression extended the replicative lifespan of fibroblasts, partly through suppression of the p53-induced microRNA miR-34a. Together these results indicate that although p53β cooperates with full-length p53 to induce senescence, Δ133p53 negatively regulates senescence-associated functions of p53.

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ORIGINAL RESEARCH PAPER

  1. Fujita, K. et al. p53 isoforms Δ133p53 and p53β are endogenous regulators of replicative cellular senescence. Nature Cell Biol. 23 Aug 2009 (doi: 10.1038/ncb1928)

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Authors
  1. Sophie Atkinson
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Atkinson, S. The more the merrier. Nat Rev Cancer 9, 688–689 (2009). https://doi.org/10.1038/nrc2737

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  • DOI: https://doi.org/10.1038/nrc2737

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