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Abrogation of the transactivation activity of p53 by BCCIP down-regulation

Xiangbing Meng1, Jingyin Yue, Zhihe Liu

  • 1Department of Molecular Genetics and Microbiology, University of New Mexico School of Medicine, Albuquerque, New Mexico 87131, USA.

The Journal of Biological Chemistry
|December 1, 2006
PubMed

Insights

The BRCA2 and CDKN1A-interacting protein (BCCIP) is essential for the tumor suppressor p53

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Cell Biology

Background:

  • The tumor suppressor protein p53's function is often lost in cancer due to mutations.
  • In cancers with wild-type p53, its activity can be impaired by unknown mechanisms.
  • Understanding these mechanisms is crucial for treating cancers with intact p53.

Purpose of the Study:

  • To identify novel mechanisms that compromise wild-type p53 transactivation activity.
  • To investigate the role of BCCIP in regulating p53 function.

Main Methods:

  • RNA interference (RNAi) was used to knock down BCCIP expression in p53 wild-type cells.
  • Assessed p53 transactivation activity, protein levels, promoter binding, and tetrameric formation.
  • Analyzed the impact of BCCIP knockdown on p53 target genes (p21 and HDM2).

Main Results:

  • BCCIP knockdown reduced p53 transactivation activity without affecting p53 protein levels.
  • BCCIP depletion inhibited p53 binding to the promoters of p21 and HDM2.
  • Reduced BCCIP levels impaired the tetrameric formation of p53.

Conclusions:

  • BCCIP plays a critical role in maintaining the transactivation activity of wild-type p53.
  • Down-regulation of BCCIP represents a novel mechanism for impairing p53 function in cancers with wild-type p53.
  • BCCIP is a potential therapeutic target in specific cancer types.

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