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Ral GTPases promote breast cancer metastasis by controlling biogenesis and organ targeting of exosomes

dc.rights.licenseopenen_US
dc.contributor.authorGHOROGHI, Shima
dc.contributor.authorMARY, Benjamin
dc.contributor.authorLARNICOL, Annabel
dc.contributor.authorASOKAN, Nandini
dc.contributor.authorKLEIN, Annick
dc.contributor.authorOSMANI, Nael
dc.contributor.authorBUSNELLI, Ignacio
dc.contributor.authorDELALANDE, Francois
dc.contributor.authorPAUL, Nicodeme
dc.contributor.authorHALARY, Sebastien
dc.contributor.authorGROS, Frederic
hal.structure.identifierLaboratoire de biogenèse membranaire [LBM]
dc.contributor.authorFOUILLEN, Laetitia
ORCID: 0000-0002-1204-9296
IDREF: 136936385
dc.contributor.authorHAEBERLE, Anne Marie
dc.contributor.authorROYER, Cathy
dc.contributor.authorSPIEGELHALTER, Coralie
dc.contributor.authorANDRE GREGOIRE, Gwennan
dc.contributor.authorMITTELHEISSER, Vincent
dc.contributor.authorDETAPPE, Alexandre
dc.contributor.authorMURPHY, Kendelle
dc.contributor.authorTIMPSON, Paul
dc.contributor.authorCARAPITO, Raphael
dc.contributor.authorBLOT CHABAUD, Marcel
dc.contributor.authorGAVARD, Julie
dc.contributor.authorCARAPITO, Christine
dc.contributor.authorVITALE, Nicolas
dc.contributor.authorLEFEBVRE, Olivier
dc.contributor.authorGOETZ, Jacky
dc.contributor.authorHYENNE, Vincent
dc.date.accessioned2022-03-11T21:56:38Z
dc.date.available2022-03-11T21:56:38Z
dc.date.issued2021
dc.identifier.issn2050084Xen_US
dc.identifier.urihttps://oskar-bordeaux.fr/handle/20.500.12278/136460
dc.description.abstractEnCancer extracellular vesicles (EVs) shuttle at distance and fertilize pre-metastatic niches facilitating subsequent seeding by tumor cells. However, the link between EV secretion mechanisms and their capacity to form pre-metastatic niches remains obscure. Using mouse models, we show that GTPases of the Ral family control, through the phospholipase D1, multi-vesicular bodies homeostasis and tune the biogenesis and secretion of pro-metastatic EVs. Importantly, EVs from RalA or RalB depleted cells have limited organotropic capacities in vivo and are less efficient in promoting metastasis. RalA and RalB reduce the EV levels of the adhesion molecule MCAM/CD146, which favors EV-mediated metastasis by allowing EVs targeting to the lungs. Finally, RalA, RalB and MCAM/CD146, are factors of poor prognosis in breast cancer patients. Altogether, our study identifies RalGTPases as central molecules linking the mechanisms of EVs secretion and cargo loading to their capacity to disseminate and induce pre-metastatic niches in a CD146 dependent manner.
dc.description.sponsorshipInfrastructure Française de Protéomique
dc.description.sponsorshipEtude des fonctions pléiotropiques de l'acide phosphatidique dans la sécrétion régulée à l'aide d'une nouvelle boite à outils moléculaires
dc.description.sponsorshipDéveloppement d'une infrastructure française distribuée pour la métabolomique dédiée à l'innovation
dc.language.isoENen_US
dc.rightsAttribution 4.0 International (CC BY 4.0)
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/
dc.subject.enZebrafish
dc.subject.enMouse
dc.subject.enHuman
dc.subject.enCell biology
dc.subject.enCancer biology
dc.title.enRal GTPases promote breast cancer metastasis by controlling biogenesis and organ targeting of exosomes
dc.typeArticle de revueen_US
dc.identifier.doi10.7554/eLife.61539en_US
dc.subject.halSciences du Vivant [q-bio]/Canceren_US
dc.identifier.pubmed33404012en_US
bordeaux.journaleLifeen_US
bordeaux.page1-29en_US
bordeaux.volume10en_US
bordeaux.hal.laboratoriesLaboratoire de Biogenèse Membranaire (LBM) - UMR 5200en_US
bordeaux.institutionUniversité de Bordeauxen_US
bordeaux.institutionCNRSen_US
bordeaux.peerReviewedouien_US
bordeaux.inpressnonen_US
bordeaux.identifier.funderIDUniversité de Strasbourg
bordeaux.identifier.funderIDInstitut national du cancer
bordeaux.identifier.funderIDLigue Contre le Cancer
bordeaux.identifier.funderIDAgence Nationale de la Recherche
bordeaux.identifier.funderIDMinistère de l'Enseignement supérieur, de la Recherche et de l'Innovation
hal.exportfalse
dc.rights.ccPas de Licence CCen_US
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