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Requirement for phosphorylation of P53 at Ser312 in suppression of chemical carcinogenesis

Elizabeth A Slee1, Xin Lu

  • 1Ludwig Institute for Cancer Research, Nuffield Department of Clinical Medicine, University of Oxford, Old Road Campus Research Building, Oxford OX3 7DQ, United Kingdom.

Scientific Reports
|November 1, 2013
PubMed

Insights

Phosphorylation of the p53 tumor suppressor on Ser312 is crucial for preventing T cell lymphomas induced by genotoxic stress. This modification enhances tumor suppression by aiding p53

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Tumor Suppressors

Background:

  • The p53 tumor suppressor protein plays a critical role in cellular response to DNA damage.
  • p53 activity is regulated by post-translational modifications, including phosphorylation.
  • Specific phosphorylation sites, like Ser312, are implicated in p53's tumor suppressive functions.

Purpose of the Study:

  • To investigate the role of p53 Ser312 phosphorylation in preventing tumor development.
  • To elucidate the mechanism by which Ser312 phosphorylation influences p53 activity and its interaction with other proteins.
  • To assess the impact of Ser312 phosphorylation on susceptibility to genotoxic agents.

Main Methods:

  • Utilized a knock-in mouse model with a Ser312 to Ala mutation in p53.
  • Administered the alkylating agent MNU and X-ray radiation to induce genotoxic stress.
  • Analyzed tumor formation, specifically T cell lymphomas, and assessed p53-E2F1 interactions and apoptosis.

Main Results:

  • p53 phosphorylation on Ser312 significantly prevents tumor induction by MNU, primarily T cell lymphomas.
  • p53(312A/A) mice exhibit increased susceptibility to X-ray-induced tumorigenesis.
  • Ser312 phosphorylation enhances p53's interaction with E2F1, promoting p53-mediated apoptosis and tumor suppression.

Conclusions:

  • Phosphorylation of p53 on Ser312 is a key mechanism for tumor suppression against genotoxic stress.
  • The interaction between p53 and E2F1, facilitated by Ser312 phosphorylation, is critical for apoptosis induction.
  • These findings highlight the importance of p53 post-translational modifications in cancer prevention.

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