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Accumulation of an inactive form of p53 protein in cells treated with TNF alpha

P Drané1, V Leblanc, F Miro-Mur

  • 1Commissariat à l'Energie Atomique, Laboratoire de Cancérogenèse Moléculaire, UMR217 CEA-CNRS, DRR, DSV, BP6 92265 Fontenay-aux-Roses Cedex, France.

Cell Death and Differentiation
|April 26, 2002
PubMed

Insights

Tumor necrosis factor alpha (TNF) causes cell cycle arrest by increasing p21/Waf1 expression, primarily through NF-kappa B activation, not p53.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Cancer Research

Background:

  • Tumor necrosis factor alpha (TNF) is a cytokine involved in inflammation and immunity.
  • TNF induces cell cycle arrest and apoptosis in various cancer cells.
  • p21/Waf1, NF-kappa B, and p53 are key regulators of cell cycle progression and stress responses.

Purpose of the Study:

  • To elucidate the roles of p53 and NF-kappa B in TNF alpha-induced G1 arrest and p21/Waf1 expression in MCF-7 cells.
  • To investigate the functional status of p53 upon TNF alpha treatment.

Main Methods:

  • MCF-7 cells were treated with TNF alpha.
  • p53 and NF-kappa B inhibition/inactivation experiments were performed.
  • p21/Waf1 mRNA levels, G1 arrest, p53 DNA-binding activity, and phosphorylation were assessed.
  • Ddb2 gene transcription rate was measured.

Main Results:

  • TNF alpha induced G1 arrest, p21/Waf1 expression, NF-kappa B activation, and p53 accumulation in MCF-7 cells.
  • p53 inhibition did not affect TNF alpha-induced p21/Waf1 mRNA accumulation.
  • NF-kappa B inactivation inhibited p21/Waf1 expression but not G1 arrest.
  • TNF alpha treatment led to p53 accumulation with increased p53 mRNA levels but without enhanced DNA-binding activity or phosphorylation at key sites.
  • Transcription of Ddb2, another p53 target gene, was not stimulated by TNF alpha.

Conclusions:

  • TNF alpha-induced p21/Waf1 expression in MCF-7 cells is primarily mediated by NF-kappa B, not p53.
  • TNF alpha treatment results in the accumulation of an inactive form of p53.
  • p53 accumulation appears to be regulated at the transcriptional level.

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