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Identification of STAG1 as a key mediator of a p53-dependent apoptotic pathway

Yoshio Anazawa1, Hirofumi Arakawa, Hidewaki Nakagawa

  • 1Laboratory of Molecular Medicine, Human Genome Center, Institute of Medical Science, University of Tokyo, 4-6-1, Shirokanedai Minato-ku, Tokyo 108-8639, Japan.

Oncogene
|September 14, 2004
PubMed

Insights

A mutant p53 protein (p53-121F) more effectively induces apoptosis. Researchers identified STAG1 as a novel p53 target gene that mediates this apoptosis, suggesting its potential for gene therapy.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Genetics

Background:

  • The tumor suppressor protein p53 plays a critical role in regulating apoptosis.
  • A mutant p53 (p53-121F) demonstrates enhanced apoptosis-inducing capabilities compared to wild-type p53 (wt-p53).

Purpose of the Study:

  • To identify apoptosis-related genes preferentially induced by the mutant p53-121F.
  • To investigate the role of STAG1 in p53-mediated apoptosis.

Main Methods:

  • cDNA microarray analysis of LS174T colon cancer cells infected with adenovirus vectors expressing p53-121F or wt-p53.
  • Analysis of STAG1 mRNA expression in response to genotoxic stress.
  • RNA-interference to suppress endogenous STAG1 expression.

Main Results:

  • STAG1 was identified as a gene with higher expression in cells infected with Ad-p53-121F compared to Ad-wtp53.
  • STAG1 expression is induced by genotoxic stress in a p53-dependent manner in multiple cancer cell lines.
  • Enforced STAG1 expression induced apoptosis, while STAG1 suppression reduced apoptosis.

Conclusions:

  • STAG1 is a novel transcriptional target of p53 that mediates p53-dependent apoptosis.
  • STAG1 shows promise as a candidate for next-generation gene therapy targeting cancer.

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