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Nrf2 Downregulation Contributes to Epithelial-to-Mesenchymal Transition in Helicobacter pylori-Infected Cells

dc.rights.licenseopenen_US
dc.contributor.authorBACON, Sarah
dc.contributor.authorSEENEEVASSEN, Lornella
dc.contributor.authorFRATACCI, Alison
dc.contributor.authorROSE, Faustine
dc.contributor.authorTIFFON, Camille
dc.contributor.authorSIFRE, Elodie
dc.contributor.authorHAYKAL, Maria M.
dc.contributor.authorMOUBARAK, Maya M.
dc.contributor.authorDUCOURNAU, Astrid
dc.contributor.authorBRUHL, Lucie
dc.contributor.authorCLAVEROL, Stephane
hal.structure.identifierChimie et Biologie des Membranes et des Nanoobjets [CBMN]
dc.contributor.authorTOKARSKI, Caroline
dc.contributor.authorGOULOUMI, Alina-Roxani
dc.contributor.authorPATERAS, Ioannis S.
dc.contributor.authorDAUBON, Thomas
dc.contributor.authorLEHOURS, Philippe
dc.contributor.authorVARON, Christine
dc.contributor.authorMARTIN, Oceane C. B.
dc.date.accessioned2023-04-26T11:39:39Z
dc.date.available2023-04-26T11:39:39Z
dc.date.issued2022-09-02
dc.identifier.issn2072-6694en_US
dc.identifier.urihttps://oskar-bordeaux.fr/handle/20.500.12278/173213
dc.description.abstractEnBackground: Gastric cancer, the fifth most common cancer worldwide, is mainly linked to Helicobacter pylori infection. H. pylori induces chronic inflammation of the gastric mucosa associated with high oxidative stress. Our study aimed at assessing the implication of Nrf2, a major regulator of cellular redox homeostasis, in H. pylori-induced gastric carcinogenesis. Methods: Using three different gastric epithelial cell lines, a non-cancerous (HFE-145) and two different subtypes of gastric cancer (AGS and MKN74), we analyzed the modulation of Nrf2 expression over time. After invalidation of Nrf2 by CRISPR-cas9, we assessed its role in H. pylori-induced epithelial-to-mesenchymal transition (EMT). Finally, we evaluated the expression of Nrf2 and ZEB1, a central EMT transcription factor, in human gastric tissues. Results: We first demonstrated that the Nrf2 signaling pathway is differentially regulated depending on the infection stage. Rapidly and transiently activated, Nrf2 was downregulated 24 h post-infection in a VacA-dependent manner. We then demonstrated that Nrf2 invalidation leads to increased EMT, which is even exacerbated after H. pylori infection. Finally, Nrf2 expression tended to decrease in human patients’ gastric mucosa infected with H. pylori. Conclusions: Our work supports the hypothesis that Nrf2 downregulation upon H. pylori infection participates in EMT, one of the most important events in gastric carcinogenesis.
dc.language.isoENen_US
dc.rightsAttribution 3.0 United States*
dc.rights.urihttp://creativecommons.org/licenses/by/3.0/us/*
dc.subject.enGastric cancer
dc.subject.enHelicobacter pylori
dc.subject.enNrf2
dc.subject.enRedox homeostasis
dc.subject.enEpithelial-to-mesenchymal transition
dc.title.enNrf2 Downregulation Contributes to Epithelial-to-Mesenchymal Transition in Helicobacter pylori-Infected Cells
dc.typeArticle de revueen_US
dc.identifier.doi10.3390/cancers14174316en_US
dc.subject.halChimie/Matériauxen_US
bordeaux.journalCancersen_US
bordeaux.volume14en_US
bordeaux.hal.laboratoriesCBMN : Chimie & de Biologie des Membranes & des Nano-objets - UMR 5248en_US
bordeaux.issue17en_US
bordeaux.institutionUniversité de Bordeauxen_US
bordeaux.institutionBordeaux INPen_US
bordeaux.institutionCNRSen_US
bordeaux.peerReviewedouien_US
bordeaux.inpressnonen_US
hal.identifierhal-04082414
hal.version1
hal.date.transferred2023-04-26T11:39:50Z
hal.exporttrue
dc.rights.ccCC BYen_US
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