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dc.contributor.authorSimón-Carrasco, Lucía
dc.contributor.authorJiménez, Gerardo
dc.contributor.authorBarbacid, Mariano 
dc.contributor.authorDrosten, Matthias 
dc.date.accessioned2019-08-22T08:20:46Z
dc.date.available2019-08-22T08:20:46Z
dc.date.issued2018-06-17
dc.identifier.citationCell Cycle. 2018;17(6):702-711.es_ES
dc.identifier.issn1538-4101es_ES
dc.identifier.urihttp://hdl.handle.net/20.500.12105/8312
dc.description.abstractThe transcriptional repressor Capicua (CIC) has emerged as an important rheostat of cell growth regulated by RAS/MAPK signaling. Cic was originally discovered in Drosophila, where it was shown to be inactivated by MAPK signaling downstream of the RTKs Torso and EGFR, which results in signal-dependent responses that are required for normal cell fate specification, proliferation and survival of developing and adult tissues. CIC is highly conserved in mammals, where it is also negatively regulated by MAPK signaling. Here, we review the roles of CIC during mammalian development, tissue homeostasis, tumor formation and therapy resistance. Available data indicate that CIC is involved in multiple biological processes, including lung development, liver homeostasis, autoimmunity and neurobehavioral processes. Moreover, CIC has been shown to be involved in tumor development as a tumor suppressor, both in human as well as in mouse models. Finally, several lines of evidence implicate CIC as a determinant of sensitivity to EGFR and MAPK pathway inhibitors, suggesting that CIC may play a broader role in human cancer than originally anticipated.es_ES
dc.description.sponsorshipThis work has been supported by grants from the Fundacio La Marato de TV3 (20131730/1) to G.J. and M.B., from the European Research Council (ERC-AG/250297-RAS AHEAD and ERC-AG/695566-THERACAN), the Autonomous Community of Madrid (S2011/BDM-2470/ONCOCYCLE) and the Foundation of the Asociacion Espanola contra el Cancer (AECC) (GC16173694BARB) to M.B, and the Spanish Ministry of Economy and Competitiveness (SAF2014-59864-R to M.B. and BFU2014-52863-P to G.J.). M.B. is the recipient of an Endowed Chair from the AXA Research Fund. L.S.C. has been supported by a fellowship from the Programa de Formacion de Personal Investigator (FPI) of the Spanish Ministry of Economy and Competitivenesses_ES
dc.language.isoenges_ES
dc.publisherTaylor & Francis es_ES
dc.relation.isversionofPostprintes_ES
dc.rights.urihttp://creativecommons.org/licenses/by-nc-sa/4.0/*
dc.subjectCICes_ES
dc.subjectEtv4es_ES
dc.subjectRas signalinges_ES
dc.subjectT-ALLes_ES
dc.subjectmouse modelses_ES
dc.titleThe Capicua tumor suppressor: a gatekeeper of Ras signaling in development and canceres_ES
dc.typeArtículoes_ES
dc.rights.licenseAtribución-NoComercial-CompartirIgual 4.0 Internacional*
dc.identifier.pubmedID29578365es_ES
dc.format.volume17es_ES
dc.format.number6es_ES
dc.format.page702-711es_ES
dc.identifier.doi10.1080/15384101.2018.1450029es_ES
dc.contributor.funderFundación La Marató TV3
dc.contributor.funderEuropean Research Council
dc.contributor.funderComunidad de Madrid 
dc.contributor.funderAsociación Española Contra el Cáncer
dc.contributor.funderFundación AXA
dc.contributor.funderMinisterio de Economía y Competividad (España)
dc.description.peerreviewedes_ES
dc.identifier.e-issn1551-4005es_ES
dc.relation.publisherversionhttps://doi.org/10.1080/15384101.2018.1450029.es_ES
dc.identifier.journalCell cycle (Georgetown, Tex.)es_ES
dc.repisalud.institucionCNIOes_ES
dc.repisalud.orgCNIOCNIO::Grupos de investigación::Grupo de Oncología Experimentales_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/EC/FP7/250297es_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/EC/H2020/695566es_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/SAF2014-59864-Res_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/BFU2014-52863-Pes_ES
dc.rights.accessRightsinfo:eu-repo/semantics/openAccesses_ES


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Atribución-NoComercial-CompartirIgual 4.0 Internacional
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