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Tau, downstream of IDH mut, inhibits the EGFR/NF-kB/TAZ mesenchymal axis, normalizing the vasculature and impairing glioma aggressiveness

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dc.contributor.authorGargini, Ricardo
dc.contributor.authorSegura Collar, Berta
dc.contributor.authorHerránz, Beatriz
dc.contributor.authorGarcía Escudero, Vega
dc.contributor.authorRomero Bravo, Andrés
dc.contributor.authorNúñez, Felipe J.
dc.contributor.authorGarcía Pérez, Daniel
dc.contributor.authorGutiérrez Guamán, Jacqueline
dc.contributor.authorAyuso Sacido, Ángel
dc.contributor.authorSeoane, Joan
dc.contributor.authorPérez Núñez, Ángel
dc.contributor.authorSepúlveda Sánchez, Juan M.
dc.contributor.authorHernández Laín, Aurelio
dc.contributor.authorCastro, María G.
dc.contributor.authorGarcía Escudero, Ramón
dc.contributor.authorÁvila, Jesús
dc.contributor.authorSánchez Gómez, Pilar
dc.contributor.departmentFarmacología
dc.contributor.otherFacultades de la UMU::Facultad de Medicina
dc.date.accessioned2026-02-19T12:51:39Z
dc.date.available2026-02-19T12:51:39Z
dc.date.issued2021-01-22
dc.description.abstractMutant IDH1/2 gliomas represent a more indolent form of cancer. However, how this group of tumors progress, in a microenvironment-dependent manner, is still a pending question. Here we describe that the expression of Tau, a gene classically associated with neurodegenerative diseases, is epigenetically controlled by the balance between wild-type and mutant IDH1/2 in gliomas. Moreover, Tau is almost absent from tumors with EGFR mutations, whereas its expression is inversely correlated with overall survival in gliomas carrying wild-type or amplified EGFR. We demonstrate that the overexpression of Tau, through the stabilization of microtubules, impairs the mesenchymal/pericyte transformation of EGFRamp/wt glioma cells through the blockade of the EGFR-NFκB-TAZ axis. However, mutant EGFR induces a constitutive activation of this pathway, which is no longer sensitive to Tau. By inhibiting the phenotypic plasticity of EGFRamp/wt glioma cells, Tau protein inhibits angiogenesis and favors vascular normalization, decreasing tumor aggressiveness.
dc.formatapplication/pdf
dc.format.extent32
dc.identifier.citationScience Translational Medicine, 2020, Vol. 12, Issue 527
dc.identifier.doihttps://doi.org/10.1126/scitranslmed.aax1501
dc.identifier.eissn1946-6242
dc.identifier.issn1946-6234
dc.identifier.urihttp://hdl.handle.net/10201/208541
dc.languageeng
dc.publisherAmerican Association for the Advancement of Science
dc.relationSin financiación externa a la Universidad
dc.relation.publisherversionhttps://www.science.org/doi/10.1126/scitranslmed.aax1501
dc.rightsAttribution 4.0 International*
dc.rights.accessRightsinfo:eu-repo/semantics/openAccess
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/*
dc.subjectTau MAPT
dc.subjectMAPT
dc.subjectEGFR
dc.subjectMicrotubule stabilizers
dc.subjectTAZ
dc.subjectNF-kB
dc.subjectCancer stem cell CSC plasticity
dc.subjectEpithelial to mesenchymal EMT transition
dc.subjectTumor derived pericytes
dc.subjectVascular normalization
dc.subjectTumor microenvironment TME
dc.subjectGlioma
dc.subject.odsNo relacionado con ningún objetivo de desarrollo sostenible
dc.titleTau, downstream of IDH mut, inhibits the EGFR/NF-kB/TAZ mesenchymal axis, normalizing the vasculature and impairing glioma aggressiveness
dc.title.alternativeThe IDH-TAU-EGFR triad defines the neovascular landscape of diffuse gliomas
dc.typeinfo:eu-repo/semantics/article
dc.type.versioninfo:eu-repo/semantics/acceptedVersion
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relation.isAuthorOfPublication.latestForDiscovery2f2500a1-1b27-4420-820c-db8c16e79afd
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