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Cold-inducible RNA-binding protein, CIRP, inhibits DNA damage-induced apoptosis by regulating p53

Hae Na Lee1, Sung-Min Ahn2, Ho Hee Jang3

  • 1Department of Molecular Medicine, Graduate School of Medicine, Lee Gil Ya Cancer and Diabetes Institute, Gachon University, Incheon 406-840, Republic of Korea.

Biochemical and Biophysical Research Communications
|July 20, 2015
PubMed

Insights

Cold-inducible RNA-binding protein (CIRP) influences apoptosis by regulating p53 levels and related gene expression. Inhibiting CIRP may offer a therapeutic strategy for cancers linked to chronic inflammation.

Area of Science:

  • Cellular Biology
  • Molecular Biology
  • Cancer Research

Background:

  • Cold-inducible RNA-binding protein (CIRP) is linked to apoptosis, but its precise mechanism is unclear.
  • Understanding CIRP's role in apoptosis is crucial for developing targeted cancer therapies, especially in inflammation-associated cancers.

Purpose of the Study:

  • To elucidate the mechanism of CIRP in DNA damage-induced apoptosis.
  • To investigate the impact of CIRP on the apoptosis pathway by modulating p53 and related gene expression.

Main Methods:

  • Conducted CIRP overexpression and knockdown experiments in cells.
  • Utilized etoposide to induce DNA damage and trigger apoptosis.
  • Analyzed the expression levels of p53, pro-apoptotic, and anti-apoptotic genes.

Main Results:

  • CIRP knockdown elevated p53, upregulating pro-apoptotic genes and downregulating anti-apoptotic genes.
  • CIRP overexpression reduced p53, downregulating pro-apoptotic genes and upregulating anti-apoptotic genes.
  • CIRP expression is upregulated by chronic inflammation, inhibiting apoptosis.

Conclusions:

  • CIRP plays a critical role in regulating apoptosis by modulating the p53 pathway.
  • CIRP's ability to inhibit apoptosis, particularly when upregulated by chronic inflammation, presents a potential therapeutic target for cancer treatment.
Keywords:
Anti-apoptotic genesApoptosisCIRPEtoposidePro-apoptotic genesp53

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