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dc.creatorTiffon, Camille
dc.creatorGiraud, Julie
dc.creatorMolina Castro, Silvia Elena
dc.creatorPeru, Sara
dc.creatorSeeneevassen, Lornella
dc.creatorSifré, Elodie
dc.creatorStaedel, Cathy
dc.creatorBessède, Emilie
dc.creatorDubus, Pierre
dc.creatorMégraud, Francis
dc.creatorLethours, Philippe
dc.creatorMartin, Océane C.B.
dc.creatorVaron, Christine
dc.date.accessioned2021-10-22T16:13:01Z
dc.date.available2021-10-22T16:13:01Z
dc.date.issued2020
dc.identifier.citationhttps://www.mdpi.com/2073-4409/9/6/1462es_ES
dc.identifier.issn2073-4409
dc.identifier.urihttps://hdl.handle.net/10669/84676
dc.description.abstractHelicobacter pylori infection, the main risk factor for gastric cancer (GC), leads to an epithelial–mesenchymal transition (EMT) of gastric epithelium contributing to gastric cancer stem cell (CSC) emergence. The Hippo pathway e ectors yes-associated protein (YAP) and transcriptional co-activator with PDZ binding motif (TAZ) control cancer initiation and progression in many cancers including GC. Here, we investigated the role of TAZ in the early steps of H. pylori-mediated gastric carcinogenesis. TAZ implication in EMT, invasion, and CSC-related tumorigenic properties were evaluated in three gastric epithelial cell lines infected by H. pylori. We showed that H. pylori infection increased TAZ nuclear expression and transcriptional enhancer TEA domain (TEAD) transcription factors transcriptional activity. Nuclear TAZ and zinc finger E-box-binding homeobox 1 (ZEB1) were co-overexpressed in cells harboring a mesenchymal phenotype in vitro, and in areas of regenerative hyperplasia in gastric mucosa of H. pylori-infected patients and experimentally infected mice, as well as at the invasive front of gastric carcinoma. TAZsilencing reduced ZEB1 expression andEMTphenotype, and strongly inhibited invasion and tumorsphere formation induced by H. pylori. In conclusion, TAZ activation in response to H. pylori infection contributes to H. pylori-induced EMT, invasion, and CSC-like tumorigenic properties. TAZ overexpression in H. pylori-induced pre-neoplastic lesions and in GC could therefore constitute a biomarker of early transformation in gastric carcinogenesis.es_ES
dc.description.sponsorshipLigue Nationale Française Contre le Cancer (French National League against Cancer)/[]//Franciaes_ES
dc.description.sponsorshipUniversidad de Costa Rica/[]/UCR/Costa Ricaes_ES
dc.description.sponsorshipMinisterio de Ciencia, Innovación, Tecnología y Telecomunicaciones/[]/MICITT/Costa Ricaes_ES
dc.description.sponsorshipFrench National Cancer Institute/[PLBio 2014-152]/INCa/Franciaes_ES
dc.description.sponsorshipLigue Contre le Cancer/[]//Franciaes_ES
dc.language.isoenges_ES
dc.sourceCells, vol.9(6), pp.1-21es_ES
dc.subjectGastric canceres_ES
dc.subjectHelicobacter pylories_ES
dc.subjectHippo pathwayes_ES
dc.subjectZEB1es_ES
dc.subjectEpithelial–mesenchymal transitiones_ES
dc.subjectTAZes_ES
dc.subjectWWTR1es_ES
dc.subjectCancer stem cellses_ES
dc.subjectYAPes_ES
dc.subjectCANCER GASTRICO - FACTORES DE RIESGOes_ES
dc.titleTAZ Controls Helicobacter pylori-Induced Epithelial–Mesenchymal Transition and Cancer Stem Cell-Like Invasive and Tumorigenic Propertieses_ES
dc.typeartículo científicoes_ES
dc.identifier.doi10.3390/cells9061462
dc.description.procedenceUCR::Vicerrectoría de Investigación::Unidades de Investigación::Ciencias de la Salud::Instituto de Investigaciones en Salud (INISA)es_ES


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