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PTPRV is a key mediator of p53-induced cell cycle exit

Gilles Doumont1, Alain Martoriati, Jean-Christophe Marine

  • 1Laboratory For Molecular Cancer Biology, Flanders Interuniversity Institute for Biotechnology (VIB), Ghent University, Ghent, Belgium.

Cell Cycle (Georgetown, Tex.)
|November 1, 2005
PubMed

Insights

The tumor suppressor p53 protein controls cell death and growth. A newly identified p53 target, Ptprv, is crucial for cell cycle exit and contact inhibition, but not apoptosis.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Cancer Research

Background:

  • The p53 tumor suppressor is a transcription factor regulating antiproliferative responses like cell cycle arrest, senescence, and apoptosis.
  • The exact transcriptional programs governed by p53 and the mechanisms dictating cell fate (survival vs. death) upon p53 activation are not fully understood.

Purpose of the Study:

  • To investigate the role of a novel direct p53 target, Ptprv (a transmembrane tyrosine phosphatase), in p53-mediated cellular responses.
  • To elucidate the function of Ptprv in cell cycle control, apoptosis, and contact inhibition.

Main Methods:

  • Identification of Ptprv as a direct p53 target.
  • Analysis of Ptprv expression in cells undergoing p53-dependent apoptosis versus cell cycle exit.
  • Assessment of p53-induced apoptosis and G1 checkpoint control in Ptprv-null mice.
  • Investigation of Ptprv induction at high cell density and its role in contact inhibition.

Main Results:

  • Ptprv expression is significantly upregulated in cells undergoing p53-dependent cell cycle exit, but not apoptosis.
  • Mice lacking Ptprv exhibit intact p53-induced apoptosis but show defects in G1 checkpoint control.
  • Ptprv is induced at high cell density and plays a role in mediating contact inhibition of cell growth.

Conclusions:

  • Ptprv is a critical mediator of p53-induced cell cycle exit.
  • Ptprv functions as a potent inhibitor of cell proliferation.
  • The findings highlight Ptprv's distinct role in regulating cell cycle arrest and contact inhibition, separate from p53-mediated apoptosis.

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