Related Experiment Video

Updated: Jun 25, 2026

A Quantitative Measurement of Reactive Oxygen Species and Senescence-associated Secretory Phenotype in Normal Human Fibroblasts During Oncogene-induced Senescence
13:59

A Quantitative Measurement of Reactive Oxygen Species and Senescence-associated Secretory Phenotype in Normal Human Fibroblasts During Oncogene-induced Senescence

Published on: August 12, 2018

The M-type receptor PLA2R regulates senescence through the p53 pathway

Arnaud Augert1, Christine Payré, Yvan de Launoit

  • 1UMR 8161, Institut de Biologie de Lille, CNRS/Universités de Lille 1 et 2/Institut Pasteur de Lille, IFR 142, 59021 Lille, France.

EMBO Reports
|February 7, 2009
PubMed

Insights

Cellular senescence, a tumor barrier, is regulated by phospholipase A2 receptor (PLA2R). Suppressing PLA2R prevents senescence, while its increase triggers premature aging, revealing PLA2R as a tumor suppressor.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Oncology

Background:

  • Cellular senescence acts as a crucial barrier against tumor development.
  • Understanding senescence escape mechanisms is vital for insights into tumorigenesis.

Purpose of the Study:

  • To identify novel genes regulating the senescence program.
  • To investigate the role of M-type receptor PLA2R in cellular senescence.

Main Methods:

  • Loss-of-function genetic screen in primary human fibroblasts.
  • Analysis of PLA2R expression and its impact on senescence.
  • Investigation of PLA2R's role in reactive oxygen species-DNA damage-p53 pathway.

Main Results:

  • Knockdown of PLA2R prevents replicative and stress-induced senescence.
  • PLA2R expression increases during replicative senescence and ectopic expression induces premature senescence.
  • PLA2R regulates senescence via a reactive oxygen species-DNA damage-p53 dependent pathway.

Conclusions:

  • PLA2R is identified as a novel regulator of cellular senescence.
  • PLA2R functions as a potential tumor suppressor gene by inducing senescence through the p53 pathway.

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