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Updated: Aug 19, 2026

Yeast As a Chassis for Developing Functional Assays to Study Human P53
14:57

Yeast As a Chassis for Developing Functional Assays to Study Human P53

Published on: August 4, 2019

COX-2 regulates p53 activity and inhibits DNA damage-induced apoptosis

Eun-Mi Choi1, Jee-In Heo, Jin-Young Oh

  • 1Department of Biochemistry and Molecular Biology, Kangwon National University College of Medicine, Chuncheon 200-701, Republic of Korea.

Biochemical and Biophysical Research Communications
|February 15, 2005
PubMed

Insights

Cyclooxygenase-2 (COX-2) directly inhibits apoptosis from DNA damage by interacting with and regulating p53 function. This finding reveals a novel mechanism for how COX-2 impacts cell death pathways and cancer progression.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Biochemistry

Background:

  • p53 protein is a key regulator of apoptosis and cell cycle arrest.
  • Cyclooxygenase-2 (COX-2) is implicated in cancer development and has been shown to inhibit apoptosis.
  • The precise molecular mechanisms by which COX-2 influences apoptosis, particularly in relation to p53, remain unclear.

Purpose of the Study:

  • To elucidate the molecular mechanisms by which COX-2 inhibits genotoxic stress-induced apoptosis.
  • To investigate the direct interaction between COX-2 and p53.
  • To determine if COX-2 modulates the transcriptional activity of p53.

Main Methods:

  • Adenoviral COX-2 overexpression system to study apoptosis inhibition.
  • Co-transfection assays to assess p53 transcriptional activity.
  • In vitro and in vivo interaction studies between COX-2 and p53.
  • Treatment with the selective COX-2 inhibitor NS-398.

Main Results:

  • COX-2 overexpression confirmed its role in inhibiting genotoxic stress-induced apoptosis.
  • COX-2 cotransfection suppressed the induction of p53 target genes, indicating regulation of p53 transcriptional function.
  • Direct physical interaction between COX-2 and p53 was observed both in vitro and in vivo.
  • The interaction between COX-2 and p53 was disrupted by NS-398 treatment.

Conclusions:

  • COX-2 directly inhibits DNA damage-induced apoptosis.
  • COX-2 exerts its anti-apoptotic function by directly interacting with and regulating p53.
  • This study uncovers a novel role for COX-2 in modulating p53 activity and influencing apoptosis.

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