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SWI/SNF complex interacts with tumor suppressor p53 and is necessary for the activation of p53-mediated transcription

Daeyoup Lee1, Jin Woo Kim, Taegun Seo

  • 1Department of Biological Sciences, Korea Advanced Institute of Science and Technology, Daejeon 305-701, Korea.

The Journal of Biological Chemistry
|April 16, 2002
PubMed

Insights

The SWI/SNF complex interacts with tumor suppressor p53, impacting gene transcription and cell cycle control. This discovery reveals a crucial molecular link for p53

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Gene Regulation

Background:

  • The SWI/SNF complex modifies nucleosome structure for gene transcription.
  • The tumor suppressor protein p53 inhibits cell growth and transformation, functions often lost in cancer.
  • Mutations in p53 are prevalent in various human cancers.

Purpose of the Study:

  • To investigate the interaction between the SWI/SNF complex and the tumor suppressor protein p53.
  • To elucidate the role of SWI/SNF subunits in p53-mediated transcriptional regulation and cellular functions.

Main Methods:

  • Genetic and biochemical analyses to detect in vivo and in vitro binding of SWI/SNF subunits to p53.
  • Overexpression studies of SWI/SNF components (hSNF5, BRG-1) and dominant-negative forms.
  • Chromatin immunoprecipitation (ChIP) assays to assess in vivo promoter recruitment.
  • Assessment of p53-mediated cell growth suppression and apoptosis.

Main Results:

  • Several human SWI/SNF complex subunits physically interact with p53.
  • Overexpression of hSNF5 and BRG-1 enhances p53 transactivation, while dominant forms repress it.
  • hSNF5 and BRG-1 are recruited to p53-dependent promoters in vivo.
  • Inhibition of p53-mediated cell growth suppression and apoptosis by dominant-negative SWI/SNF forms.

Conclusions:

  • The SWI/SNF complex is essential for p53-driven transcriptional activation.
  • The SWI/SNF complex plays a significant role in p53-mediated cell cycle control and tumor suppression.
  • This molecular connection highlights the SWI/SNF complex as a potential target in cancer therapies involving p53 dysfunction.

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