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dc.contributor.authorRabé, Marion
dc.contributor.authorFonteneau, Lucie
dc.contributor.authorOliver, Lisa
dc.contributor.authorMorales-Molina, Alvaro 
dc.contributor.authorJubelin, Camille
dc.contributor.authorGarcia-Castro, Javier 
dc.contributor.authorHeymann, Dominique
dc.contributor.authorGratas, Catherine
dc.contributor.authorVallette, François M.
dc.date.accessioned2022-05-30T12:33:28Z
dc.date.available2022-05-30T12:33:28Z
dc.date.issued2022-05-25
dc.identifier.citationFront Cell Dev Biol. 2022 May 25;10:835273.es_ES
dc.identifier.urihttp://hdl.handle.net/20.500.12105/14571
dc.descriptionFactor de impacto: 6,684 Q1.
dc.description.abstractWe have observed a drug-tolerant/persister state in a human glioblastoma (GBM) cell line after exposure to temozolomide, the standard-of-care chemotherapeutic agent for GBM. We used a multicolor lentiviral genetic barcode labeling to follow cell population evolution during temozolomide treatment. We observed no change in the distribution of the different colored populations of cells in persister or resistant cells suggesting that pre-existing minor subpopulations, which would be expected to be restricted to a single color, were not amplified/selected during the response to the drug. We have previously identified four genes (CHI3L1, FAT2, KLK5, and HB-EGF) that were over-expressed during the persister stage. Single-cell analysis of these four genes indicated that they were expressed in different individual cells ruling out the existence of a single persister-specific clone but suggesting rather a global answer. Even so, the transitory silencing of CHI3L1, FAT2, or KLK5 influenced the expression of the other three genes and the survival of U251 cells in absence of temozolomide. Since proteins encoded by the four genes are all localized in the extracellular matrix or interact within the extracellular compartment, we propose that cellular interactions and communications are important during the persister stage before the acquisition of chemo-resistance. Thus, persisters might be a new therapeutically relevant target in GBM.es_ES
dc.description.sponsorshipThis research was founded by a grant from the “Ligue contre le Cancer-Grand Ouest” and a Région Pays de la Loire special fund (ERRATA program).es_ES
dc.language.isoenges_ES
dc.publisherFrontiers Media es_ES
dc.type.hasVersionVoRes_ES
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/*
dc.subjectGliomaes_ES
dc.subjectPersisterses_ES
dc.subjectCloneses_ES
dc.subjectResistancees_ES
dc.subjectBarcodinges_ES
dc.titleCellular Heterogeneity and Cooperativity in Glioma Persister Cells Under Temozolomide Treatmentes_ES
dc.typejournal articlees_ES
dc.rights.licenseAttribution 4.0 International*
dc.format.volume10es_ES
dc.format.page835273es_ES
dc.identifier.doi10.3389/fcell.2022.835273es_ES
dc.contributor.funderLigue Nationale Contre le Cancer (Francia) es_ES
dc.description.peerreviewedes_ES
dc.identifier.e-issn2296-634Xes_ES
dc.relation.publisherversionhttps://doi.org/10.3389/fcell.2022.835273es_ES
dc.identifier.journalFrontiers in Cell and Developmental Biologyes_ES
dc.repisalud.centroISCIII::Instituto de Investigación de Enfermedades Rarases_ES
dc.repisalud.institucionISCIIIes_ES
dc.rights.accessRightsopen accesses_ES


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