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Research Paper|Volume 6, Issue 11|pp 921—930

TAp73 promotes anti-senescence-anabolism not proliferation

Massimiliano Agostini1,2, Maria Victoria Niklison-Chirou1,5, Maria Valeria Catani2, Richard A. Knight1, Gerry Melino1,2,3, Alessandro Rufini1,2,4
  • 1Medical Research Council, Toxicology Unit, Leicester LE1 9HN, UK
  • 2Department of Experimental Medicine and Surgery, University of Rome “Tor Vergata”, 00133 Rome, Italy
  • 3Biochemistry Laboratory IDI-IRCC, c/o Department of Experimental Medicine and Surgery, University of Rome “Tor Vergata”, 00133 Rome, Italy
  • 4Department of Cancer Studies and Molecular Medicine, University of Leicester, Leicester UK
  • 5Blizard Institute of Cell and Molecular Science, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London, E1 2AT, UK; current address
Received: October 27, 2014Accepted: November 11, 2014Published: November 13, 2014
https://doi.org/10.18632/aging.100701

Copyright: © 2014 Agostini et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

TAp73, a member of the p53 family, has been traditionally considered a tumor suppressor gene, but a recent report has claimed that it can promote cellular proliferation. This assumption is based on biochemical evidence of activation of anabolic metabolism, with enhanced pentose phosphate shunt (PPP) and nucleotide biosynthesis. Here, while we confirm that TAp73 expression enhances anabolism, we also substantiate its role in inhibiting proliferation and promoting cell death. Hence, we would like to propose an alternative interpretation of the accumulating data linking p73 to cellular metabolism: we suggest that TAp73 promotes anabolism to counteract cellular senescence rather than to support proliferation.