Abstract:
:Senescence is a stable proliferative arrest induced by various stresses such as telomere erosion, oncogenic or oxidative stress. Compelling evidence suggests that it acts as a barrier against tumour development. Describing new mechanisms that favour an escape from senescence can thus reveal new insights into tumorigenesis. To identify new genes controlling the senescence programme, we performed a loss-of-function genetic screen in primary human fibroblasts. We report that knockdown of the M-type receptor PLA2R (phospholipase A2 receptor) prevents the onset of replicative senescence and diminishes stress-induced senescence. Interestingly, expression of PLA2R increases during replicative senescence, and its ectopic expression results in premature senescence. We show that PLA2R regulates senescence in a reactive oxygen species-DNA damage-p53-dependent manner. Taken together, our study identifies PLA2R as a potential new tumour suppressor gene crucial in the induction of cellular senescence through the activation of the p53 pathway.
journal_name
EMBO Repjournal_title
EMBO reportsauthors
Augert A,Payré C,de Launoit Y,Gil J,Lambeau G,Bernard Ddoi
10.1038/embor.2008.255subject
Has Abstractpub_date
2009-03-01 00:00:00pages
271-7issue
3eissn
1469-221Xissn
1469-3178pii
embor2008255journal_volume
10pub_type
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