The M-type receptor PLA2R regulates senescence through the p53 pathway
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 insi...
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| Veröffentlicht in: | EMBO reports 2009-03, Vol.10 (3), p.271-277 |
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| creator | Augert, Arnaud Payré, Christine de Launoit, Yvan Gil, Jesus Lambeau, Gérard Bernard, David |
| description | 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. |
| doi_str_mv | 10.1038/embor.2008.255 |
| format | Article |
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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.</description><identifier>ISSN: 1469-221X</identifier><identifier>EISSN: 1469-3178</identifier><identifier>EISSN: 1469-221X</identifier><identifier>DOI: 10.1038/embor.2008.255</identifier><identifier>PMID: 19197340</identifier><identifier>CODEN: ERMEAX</identifier><language>eng</language><publisher>Chichester, UK: John Wiley & Sons, Ltd</publisher><subject>Aging ; Animals ; Autoantibodies ; Blotting, Western ; Cancer ; Cell Aging ; Cell Line ; Cellular Senescence - physiology ; Chi-Square Distribution ; Deoxyribonucleic acid ; DNA ; DNA damage ; Down-Regulation ; EMBO06 ; EMBO24 ; Epitopes ; Fibroblasts ; Fibroblasts - cytology ; Fibroblasts - physiology ; Gene Knockdown Techniques ; Genetics ; Glomerulonephritis, Membranous ; Humans ; Immunoglobulin G ; Kidney Glomerulus ; Life Sciences ; Mass Spectrometry ; Molecular biology ; Oncology ; Oxidative stress ; p53 ; PLA2R ; Reactive Oxygen Species ; Reactive Oxygen Species - metabolism ; Receptors, Phospholipase A2 ; Receptors, Phospholipase A2 - genetics ; Receptors, Phospholipase A2 - metabolism ; Scientific Report ; senescence ; Signal Transduction ; Signal Transduction - physiology ; Tumor Suppressor Protein p53 ; Tumor Suppressor Protein p53 - genetics ; Tumor Suppressor Protein p53 - metabolism ; Tumors</subject><ispartof>EMBO reports, 2009-03, Vol.10 (3), p.271-277</ispartof><rights>European Molecular Biology Organization 2009</rights><rights>Copyright © 2009 European Molecular Biology Organization</rights><rights>Copyright Nature Publishing Group Mar 2009</rights><rights>Distributed under a Creative Commons Attribution 4.0 International License</rights><rights>Copyright © 2009, European Molecular Biology Organization 2009</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c6725-c6fd7dfa1b2a99f621dda8f48bd5c3a2d014d298e4e456db33894ae5fb255a653</citedby><cites>FETCH-LOGICAL-c6725-c6fd7dfa1b2a99f621dda8f48bd5c3a2d014d298e4e456db33894ae5fb255a653</cites><orcidid>0000-0002-4303-6260 ; 0000-0002-1557-2074 ; 0000-0002-9239-518X</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2658567/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2658567/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,724,777,781,882,1412,1428,27905,27906,45555,45556,46390,46814,53772,53774</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19197340$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://hal.science/hal-00417702$$DView record in HAL$$Hfree_for_read</backlink></links><search><creatorcontrib>Augert, Arnaud</creatorcontrib><creatorcontrib>Payré, Christine</creatorcontrib><creatorcontrib>de Launoit, Yvan</creatorcontrib><creatorcontrib>Gil, Jesus</creatorcontrib><creatorcontrib>Lambeau, Gérard</creatorcontrib><creatorcontrib>Bernard, David</creatorcontrib><title>The M-type receptor PLA2R regulates senescence through the p53 pathway</title><title>EMBO reports</title><addtitle>EMBO Rep</addtitle><addtitle>EMBO Rep</addtitle><description>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. 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Academic</collection><collection>Hyper Article en Ligne (HAL)</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>EMBO reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Augert, Arnaud</au><au>Payré, Christine</au><au>de Launoit, Yvan</au><au>Gil, Jesus</au><au>Lambeau, Gérard</au><au>Bernard, David</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The M-type receptor PLA2R regulates senescence through the p53 pathway</atitle><jtitle>EMBO reports</jtitle><stitle>EMBO Rep</stitle><addtitle>EMBO Rep</addtitle><date>2009-03</date><risdate>2009</risdate><volume>10</volume><issue>3</issue><spage>271</spage><epage>277</epage><pages>271-277</pages><issn>1469-221X</issn><eissn>1469-3178</eissn><eissn>1469-221X</eissn><coden>ERMEAX</coden><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. 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| subjects | Aging Animals Autoantibodies Blotting, Western Cancer Cell Aging Cell Line Cellular Senescence - physiology Chi-Square Distribution Deoxyribonucleic acid DNA DNA damage Down-Regulation EMBO06 EMBO24 Epitopes Fibroblasts Fibroblasts - cytology Fibroblasts - physiology Gene Knockdown Techniques Genetics Glomerulonephritis, Membranous Humans Immunoglobulin G Kidney Glomerulus Life Sciences Mass Spectrometry Molecular biology Oncology Oxidative stress p53 PLA2R Reactive Oxygen Species Reactive Oxygen Species - metabolism Receptors, Phospholipase A2 Receptors, Phospholipase A2 - genetics Receptors, Phospholipase A2 - metabolism Scientific Report senescence Signal Transduction Signal Transduction - physiology Tumor Suppressor Protein p53 Tumor Suppressor Protein p53 - genetics Tumor Suppressor Protein p53 - metabolism Tumors |
| title | The M-type receptor PLA2R regulates senescence through the p53 pathway |
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