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p21 delays tumor onset by preservation of chromosomal stability

Juan A Barboza1, Geng Liu, Zhenlin Ju

  • 1Department of Cancer Genetics and Pathology, University of Texas M. D. Anderson Cancer Center, 1515 Holcombe Boulevard, Houston, TX 77030, USA.

Proceedings of the National Academy of Sciences of the United States of America
|December 16, 2006
PubMed

Insights

The tumor suppressor p53 normally prevents cancer. A p53 mutant (p53R172P) delays tumor onset, but its function requires p21 to maintain genome stability and cell cycle arrest.

Area of Science:

  • Molecular Biology
  • Genetics
  • Cancer Research

Background:

  • The p53 protein is a critical tumor suppressor, inducing cell cycle arrest and apoptosis in response to DNA damage.
  • A specific p53 mutant, p53R172P, retains cell cycle arrest but lacks apoptosis function, delaying tumor development in mice with stable genomes.

Purpose of the Study:

  • To investigate the role of p21 in the tumor-suppressive functions of the p53 mutant p53R172P.
  • To determine if p21 is essential for maintaining chromosomal stability and delaying tumor onset in mice carrying the p53R172P mutation.

Main Methods:

  • Crossed Trp53(515C/515C) mice (encoding p53R172P) with p21-null mice.
  • Assessed cell cycle arrest function of p53R172P.
  • Performed cytogenetic examination of tumors (sarcomas and lymphomas) from the generated mouse models.

Main Results:

  • Loss of p21 completely abrogated the cell cycle arrest function of p53R172P.
  • Tumor onset was accelerated in Trp53(515C/515C) mice lacking p21.
  • Tumors from Trp53(515C/515C) p21(-/-) mice exhibited aneuploidy and chromosomal aberrations, unlike those from Trp53(515C/515C) mice.

Conclusions:

  • p21 is crucial for p53-mediated checkpoint control and preservation of chromosomal stability.
  • p21 cooperates with apoptosis in suppressing tumor onset, highlighting its essential role alongside the p53 pathway.

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