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dc.contributor.authorSegura-Collar, Berta 
dc.contributor.authorGargini, Ricardo 
dc.contributor.authorTovar-Ambel, Elena 
dc.contributor.authorHernandez-Sanmiguel, Esther 
dc.contributor.authorEpifano, Carolina 
dc.contributor.authorPerez de Castro, Ignacio 
dc.contributor.authorHernández-Laín, Aurelio
dc.contributor.authorCasas-Tintó, Sergio
dc.contributor.authorSánchez-Gómez, Pilar 
dc.date.accessioned2020-02-12T12:24:45Z
dc.date.available2020-02-12T12:24:45Z
dc.date.issued2020-01-14
dc.identifier.citationCancers (Basel). 2020 Jan 14;12(1). pii: E208.es_ES
dc.identifier.issn2072-6694es_ES
dc.identifier.urihttp://hdl.handle.net/20.500.12105/9083
dc.description.abstractDespite the high frequency of EGFR and TP53 genetic alterations in gliomas, little is known about their crosstalk during tumor progression. Here, we described a mutually exclusive distribution between mutations in these two genes. We found that wild-type p53 gliomas are more aggressive than their mutant counterparts, probably because the former accumulate amplifications and/or mutations in EGFR and show a stronger activation of this receptor. In addition, we identified a series of genes associated with vesicular trafficking of EGFR in p53 wild-type gliomas. Among these genes, TMEM167A showed the strongest implication in overall survival in this group of tumors. In agreement with this observation, inhibition of TMEM167A expression impaired the subcutaneous and the intracranial growth of wild-type p53 gliomas, regardless of the presence of EGFR mutations. In the absence of p53 mutations, TMEM167A knockdown reduced the acidification of intracellular vesicles, affecting the autophagy process and impairing EGFR trafficking and signaling. This effect was mimicked by an inhibitor of the vacuolar ATPase. We propose that the increased aggressiveness of wild-type p53 gliomas might be due to the increase in growth factor signaling activity, which depends on the regulation of vesicular trafficking by TMEM167A.es_ES
dc.description.sponsorshipThis research was funded by the Ministerio de Economía y Competitividad: (Acción Estratégica en Salud) grants: PI13/01258 to AHL; by “Asociación Española contra el Cancer” (AECC) grants: Junior Researcher to RG; and by Ministerio de Economía y Competitividad: SAF2015-65175-R/FEDER to PSG.es_ES
dc.language.isoenges_ES
dc.publisherMultidisciplinary Digital Publishing Institute (MDPI) es_ES
dc.type.hasVersionVoRes_ES
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/*
dc.subjectEGFR/AKT signalinges_ES
dc.subjectAutophagyes_ES
dc.subjectGliomaes_ES
dc.subjectMutant p53es_ES
dc.subjectVesicular traffickinges_ES
dc.subjectWild-type p53es_ES
dc.titleThe EGFR-TMEM167A-p53 Axis Defines the Aggressiveness of Gliomases_ES
dc.typejournal articlees_ES
dc.rights.licenseAtribución 4.0 Internacional*
dc.identifier.pubmedID31947645es_ES
dc.format.volume12es_ES
dc.format.number1es_ES
dc.format.page208es_ES
dc.identifier.doi10.3390/cancers12010208es_ES
dc.contributor.funderMinisterio de Economía y Competitividad (España) 
dc.contributor.funderAsociación Española Contra el Cáncer 
dc.description.peerreviewedes_ES
dc.relation.publisherversionhttps://doi.org/10.3390/cancers12010208es_ES
dc.identifier.journalCancerses_ES
dc.repisalud.centroISCIII::Centro Nacional de Microbiologíaes_ES
dc.repisalud.centroISCIII::Instituto de Investigación de Enfermedades Rarases_ES
dc.repisalud.institucionISCIIIes_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/PI13/01258es_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/SAF2015-65175-R/FEDERes_ES
dc.rights.accessRightsopen accesses_ES


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Atribución 4.0 Internacional
Este Item está sujeto a una licencia Creative Commons: Atribución 4.0 Internacional