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TRAIL receptor gene editing unveils TRAIL-R1 as a master player of apoptosis induced by TRAIL and ER stress

dc.relation.isnodouble1c034e30-28f7-43c3-aeee-5b0c823b63ce*
dc.relation.isnodouble1c13e70a-1fac-4a77-8d61-6e9bdb663740*
dc.relation.isnodoublee5e9d18a-7eda-4c43-8618-4b2be9d89a4a*
dc.contributor.authorDUFOUR, Florent
dc.contributor.authorRATTIER, Thibault
dc.contributor.authorCONSTANTINESCU, Andrei Alexandru
dc.contributor.authorZISCHLER, Luciana
dc.contributor.authorMORLE, Aymeric
dc.contributor.authorBEN MABROUK, Hazem
dc.contributor.authorHUMBLIN, Etienne
dc.contributor.authorJACQUEMIN, Guillaume
dc.contributor.authorSZEGEZDI, Eva
dc.contributor.authorDELACOTE, Fabien
dc.contributor.authorMARRAKCHI, Naziha
hal.structure.identifierChimie et Biologie des Membranes et des Nanoobjets [CBMN]
dc.contributor.authorGUICHARD, Gilles
dc.contributor.authorPELLAT-DECEUNYNCK, Catherine
hal.structure.identifierInstitut Bergonié [Bordeaux]
dc.contributor.authorVACHER, Pierre
dc.contributor.authorLEGEMBRE, Patrick
dc.contributor.authorGARRIDO, Carmen
dc.contributor.authorMICHEAU, Olivier
dc.date.accessioned2020-07-09T14:16:58Z
dc.date.available2020-07-09T14:16:58Z
dc.date.issued2017
dc.identifier.issn1949-2553
dc.identifier.urihttps://oskar-bordeaux.fr/handle/20.500.12278/10331
dc.description.abstractEnTRAIL induces selective tumor cell death through TRAIL-R1 and TRAIL-R2. Despite the fact that these receptors share high structural homologies, induction of apoptosis upon ER stress, cell autonomous motility and invasion have solely been described to occur through TRAIL-R2. Using the TALEN gene-editing approach, we show that TRAIL-R1 can also induce apoptosis during unresolved unfolded protein response (UPR). Likewise, TRAIL-R1 was found to co-immunoprecipitate with FADD and caspase-8 during ER stress. Its deficiency conferred resistance to apoptosis induced by thaspigargin, tunicamycin or brefeldin A. Our data also demonstrate that tumor cell motility and invasion-induced by TRAIL-R2 is not cell autonomous but induced in a TRAIL-dependant manner. TRAIL-R1, on the other hand, is unable to trigger cell migration owing to its inability to induce an increase in calcium flux. Importantly, all the isogenic cell lines generated in this study revealed that apoptosis induced TRAIL is preferentially induced by TRAIL-R1. Taken together, our results provide novel insights into the physiological functions of TRAIL-R1 and TRAIL-R2 and suggest that targeting TRAIL-R1 for anticancer therapy is likely to be more appropriate owing to its lack of pro-motile signaling capability.
dc.title.enTRAIL receptor gene editing unveils TRAIL-R1 as a master player of apoptosis induced by TRAIL and ER stress
dc.typeArticle de revue
dc.identifier.doi10.18632/oncotarget.14285
dc.subject.halChimie/Matériaux
bordeaux.journalOncotarget
bordeaux.page9974-9985
bordeaux.volume8
bordeaux.hal.laboratoriesInstitut de Chimie & de Biologie des Membranes & des Nano-objets (CBMN) - UMR 5248*
bordeaux.hal.laboratoriesInstitut de Chimie & de Biologie des Membranes & des Nano-objets (CBMN, UMR 5248)
bordeaux.issue6
bordeaux.institutionUniversité de Bordeaux
bordeaux.institutionBordeaux INP
bordeaux.COinSctx_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.jtitle=Oncotarget&rft.date=2017&rft.volume=8&rft.issue=6&rft.spage=9974-9985&rft.epage=9974-9985&rft.eissn=1949-2553&rft.issn=1949-2553&rft.au=DUFOUR,%20Florent&RATTIER,%20Thibault&CONSTANTINESCU,%20Andrei%20Alexandru&ZISCHLER,%20Luciana&MORLE,%20Aymeric&rft.genre=article


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