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Transcription factor p63, a member of the p53 family of tumour suppressors, regulates hepatic glucose metabolism
  1. Gilles Mithieux
  1. Institut National de la Santé et de la Recherche Médicale U1213, University Lyon 1 Faculty of Medicine Lyon-Est, Lyon, France
  1. Correspondence to Dr Gilles Mithieux, University Lyon 1 Faculty of Medicine Lyon-Est, Lyon, France; gilles.mithieux{at}univ-lyon1.fr

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Transcription factors of the family p53 have emerged as an important set of tumour suppressors, able to regulate various cell functions like cell cycle arrest, differentiation, DNA repair, apoptosis that can all modulate the initiation or the progression of tumours.1 The close relationships between the biochemical pathways that regulate cell metabolism and cancer initiation are becoming increasingly well known.2 Consistently, out of the family, p53 has been reported to regulate body glucose metabolism, e.g. insulin sensitivity of the adipose tissue3 or hepatic gluconeogenesis and glycogen storage.4 Curiously, there was not much information about the role in the control of metabolism of p63, another key member of the family. However, the observation that mice lacking p63 develop obesity and altered glucose control and insulin resistance has suggested that this could be the case.5

P63 is widely expressed and exerts various cell-specific effects. Therefore, it is not possible to get firm conclusions on the precise metabolic mechanisms it may control from a global KO.5 In Gut, Gonzalez-Rellan et al used a mouse model of liver-specific deletion of p63 to decipher the mechanisms by which the factor modulates …

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Footnotes

  • Contributors GM analysed the related paper and bibliography and wrote the commentary.

  • Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

  • Competing interests None declared.

  • Provenance and peer review Commissioned; internally peer reviewed.

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