Research Paper Volume 6, Issue 11 pp 921—930
TAp73 promotes anti-senescence-anabolism not proliferation
- 1 Medical Research Council, Toxicology Unit, Leicester LE1 9HN, UK
- 2 Department of Experimental Medicine and Surgery, University of Rome “Tor Vergata”, 00133 Rome, Italy
- 3 Biochemistry Laboratory IDI-IRCC, c/o Department of Experimental Medicine and Surgery, University of Rome “Tor Vergata”, 00133 Rome, Italy
- 4 Department of Cancer Studies and Molecular Medicine, University of Leicester, Leicester UK
- 5 Blizard 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, 2014 Accepted: November 11, 2014 Published: November 13, 2014
https://doi.org/10.18632/aging.100701How to Cite
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.
Abbreviations
GC: Gas chromatography; MS: Mass Spectrometry; LC: Liquid chromatography; DMED: Dulbecco minimal essential medium; FBS: foetal bovine serum.