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p73 is a p53-independent, Sp1-dependent repressor of cyclin B1 transcription

Steven A Innocente1, Jonathan M Lee

  • 1Hamilton Regional Cancer Centre, Hamilton, Ontario, Canada.

Biochemical and Biophysical Research Communications
|March 2, 2005
PubMed

Insights

The p53 protein family, including p73, regulates cell growth. p73 isoforms, p73alpha and p73beta, inhibit cyclin B1 gene expression, suggesting a role in cell cycle control and cancer prevention.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Genetics

Background:

  • The p53 protein family (p53, p63, p73) is crucial for cell growth and differentiation.
  • p53's role in preventing G2/M transition by regulating cyclin B1 suggests a G2 checkpoint's role in preventing cancer.

Purpose of the Study:

  • To investigate the transcriptional regulatory role of p73 isoforms (p73alpha and p73beta) on cyclin B1.
  • To determine if p73 shares p53's ability to repress cyclin B1 transcription.

Main Methods:

  • Assessing the effect of p73alpha and p73beta expression on cyclin B1 mRNA and protein levels.
  • Analyzing cyclin B1 promoter activity in the presence of p73 isoforms.
  • Investigating the dependence of p73-mediated repression on Sp1 and NF-Y binding sites.

Main Results:

  • p73alpha and p73beta expression decreased cyclin B1 mRNA levels and attenuated cyclin B1 promoter activity.
  • This repression occurred in both p53-deficient and p53-containing cells.
  • p73-mediated repression of the cyclin B1 promoter required functional Sp1-binding sites and was independent of NF-Y sites.

Conclusions:

  • p73 isoforms possess the ability to transcriptionally repress cyclin B1, similar to p53.
  • p73 likely mediates this repression through the Sp1 transcription factor.
  • These findings highlight p73's role in cell cycle regulation and its potential in preventing neoplastic transformation.

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