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dc.contributor.authorSoulet, Fabiennees_ES
dc.contributor.authorBodineau, Clémentes_ES
dc.contributor.authorHooks, Katarzyna B.es_ES
dc.contributor.authorDescarpentrie, Jeanes_ES
dc.contributor.authorAlves, Isabeles_ES
dc.contributor.authorDubreuil, Mariellees_ES
dc.contributor.authorMouchard, Amandinees_ES
dc.contributor.authorEugenie, Malauriees_ES
dc.contributor.authorHoepffner, Jean-Luces_ES
dc.contributor.authorLópez, Jose J.es_ES
dc.contributor.authorRosado, Juan A.es_ES
dc.contributor.authorSoubeyran, Isabellees_ES
dc.contributor.authorTomé, Mercedeses_ES
dc.contributor.authorDurán, Raúl V.es_ES
dc.contributor.authorNikolski, Machaes_ES
dc.contributor.authorVilloutreix, Bruno O.es_ES
dc.contributor.authorEvrard, Sergees_ES
dc.contributor.authorSiegfried, Geraldinees_ES
dc.contributor.authorKhatib, Abdel-Majides_ES
dc.date.accessioned2020-10-15T09:21:48Z-
dc.date.available2020-10-15T09:21:48Z-
dc.date.issued2020-
dc.identifier.citationJCI Insight 5(14): e129070 (2020)es_ES
dc.identifier.urihttp://hdl.handle.net/10261/221229-
dc.description.abstractApelin is a well-established mediator of survival and mitogenic signaling through the apelin receptor (Aplnr) and has been implicated in various cancers; however, little is known regarding Elabela (ELA/APELA) signaling, also mediated by Aplnr, and its role and the role of the conversion of its precursor proELA into mature ELA in cancer are unknown. Here, we identified a function of mTORC1 signaling as an essential mediator of ELA that repressed kidney tumor cell growth, migration, and survival. Moreover, sunitinib and ELA showed a synergistic effect in repressing tumor growth and angiogenesis in mice. The use of site-directed mutagenesis and pharmacological experiments provided evidence that the alteration of the cleavage site of proELA by furin induced improved ELA antitumorigenic activity. Finally, a cohort of tumors and public data sets revealed that ELA was only repressed in the main human kidney cancer subtypes, namely clear cell, papillary, and chromophobe renal cell carcinoma. Aplnr was expressed by various kidney cells, whereas ELA was generally expressed by epithelial cells. Collectively, these results showed the tumor-suppressive role of mTORC1 signaling mediated by ELA and established the potential use of ELA or derivatives in kidney cancer treatment.es_ES
dc.description.sponsorshipThis work was supported by INSERM, SIRIC Brio, Region Nouvelle Aquitaine, and La Ligue Contre le Cancer.es_ES
dc.language.isoenges_ES
dc.publisherAmerican Society for Clinical Investigationes_ES
dc.relation.isversionofPublisher's versiones_ES
dc.rightsopenAccesses_ES
dc.titleELA/APELA precursor cleaved by furin displays tumor suppressor function in renal cell carcinoma through mTORC1 activationes_ES
dc.typeartículoes_ES
dc.identifier.doihttp://dx.doi.org/10.1172/jci.insight.129070-
dc.description.peerreviewedPeer reviewedes_ES
dc.relation.publisherversionhttps://doi.org/10.1172/jci.insight.129070es_ES
dc.identifier.e-issn2379-3708-
dc.contributor.funderLigue Nationale contre le Cancer (France)es_ES
dc.contributor.funderConseil régional d'Aquitainees_ES
dc.relation.csices_ES
oprm.item.hasRevisionno ko 0 false*
dc.identifier.funderhttp://dx.doi.org/10.13039/501100009468es_ES
dc.identifier.funderhttp://dx.doi.org/10.13039/501100004099es_ES
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