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Oncogenic dependence of glioma cells on kish/TMEM167A regulation of vesicular trafficking

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dc.contributor.authorPortela, Marta
dc.contributor.authorSegura-Collar, Berta
dc.contributor.authorArgudo, Irene
dc.contributor.authorSáiz, Almudena
dc.contributor.authorGargini, Ricardo
dc.contributor.authorSánchez-Gómez, Pilar
dc.contributor.authorCasas-Tintó, Sergio
dc.contributor.funderMinisterio de Economía y Competitividad (España)
dc.contributor.funderMinisterio de Ciencia e Innovación (España)
dc.contributor.funderAsociación Española Contra el Cáncer
dc.date.accessioned2020-07-16T09:32:33Z
dc.date.available2020-07-16T09:32:33Z
dc.date.issued2019
dc.description.abstractGenetic lesions in glioblastoma (GB) include constitutive activation of PI3K and EGFR pathways to drive cellular proliferation and tumor malignancy. An RNAi genetic screen, performed in Drosophila melanogaster to discover new modulators of GB development, identified a member of the secretory pathway: kish/TMEM167A. Downregulation of kish/TMEM167A impaired fly and human glioma formation and growth, with no effect on normal glia. Glioma cells increased the number of recycling endosomes, and reduced the number of lysosomes. In addition, EGFR vesicular localization was primed toward recycling in glioma cells. kish/TMEM167A downregulation in gliomas restored endosomal system to a physiological state and altered lysosomal function, fueling EGFR toward degradation by the proteasome. These endosomal effects mirrored the endo/lysosomal response of glioma cells to Brefeldin A (BFA), but not the Golgi disruption and the ER collapse, which are associated with the undesirable toxicity of BFA in other cancers. Our results suggest that glioma growth depends on modifications of the vesicle transport system, reliant on kish/TMEM167A. Noncanonical genes in GB could be a key for future therapeutic strategies targeting EGFR-dependent gliomas.es_ES
dc.description.peerreviewedNoes_ES
dc.format.number2es_ES
dc.format.page404-417es_ES
dc.format.volume67es_ES
dc.identifier.citationGlia . 2019 Feb;67(2):404-417es_ES
dc.identifier.doi10.1002/glia.23551es_ES
dc.identifier.e-issn1098-1136es_ES
dc.identifier.journalGliaes_ES
dc.identifier.pubmedID30506943es_ES
dc.identifier.urihttp://hdl.handle.net/20.500.12105/10787
dc.language.isoenges_ES
dc.publisherWileyes_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/SAF2015-65175-R
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/BFU2015-65685P
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/IJCI-2014-19272
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/RYC-2012-11410
dc.relation.publisherversionhttps://doi.org/10.1002/glia.23551es_ES
dc.repisalud.centroISCIII::Unidad Funcional de Investigación de Enfermedades Crónicas (UFIEC)es_ES
dc.repisalud.institucionISCIIIes_ES
dc.rights.accessRightsopen accesses_ES
dc.rights.licenseAtribución-NoComercial-CompartirIgual 4.0 Internacional*
dc.rights.urihttp://creativecommons.org/licenses/by-nc-sa/4.0/*
dc.subject.meshAnimalses_ES
dc.subject.meshAnimals, Genetically Modifiedes_ES
dc.subject.meshBraines_ES
dc.subject.meshBrain Neoplasmses_ES
dc.subject.meshCell Line, Tumores_ES
dc.subject.meshDisease Models, Animales_ES
dc.subject.meshDrosophila Proteinses_ES
dc.subject.meshDrosophila melanogasteres_ES
dc.subject.meshEnzyme Inhibitorses_ES
dc.subject.meshErbB Receptorses_ES
dc.subject.meshFemalees_ES
dc.subject.meshGene Expression Regulation, Neoplastices_ES
dc.subject.meshGliomaes_ES
dc.subject.meshHeterograftses_ES
dc.subject.meshHumanses_ES
dc.subject.meshLeupeptinses_ES
dc.subject.meshLuminescent Proteinses_ES
dc.subject.meshMalees_ES
dc.subject.meshMicees_ES
dc.subject.meshProtein Transportes_ES
dc.subject.meshRNA Interferencees_ES
dc.titleOncogenic dependence of glioma cells on kish/TMEM167A regulation of vesicular traffickinges_ES
dc.typepreprintes_ES
dc.type.hasVersionSMURes_ES
dspace.entity.typePublication
relation.isAuthorOfPublication1a36f06c-e520-427d-90a4-53617c60d520
relation.isAuthorOfPublication7e71ffd7-1cca-494f-b9ae-684e04d9746e
relation.isAuthorOfPublication5149e567-93ff-423f-86af-68545f9abee7
relation.isAuthorOfPublication.latestForDiscovery1a36f06c-e520-427d-90a4-53617c60d520
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