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dc.contributor.authorFloch, Pauline
dc.contributor.authorCapdevielle, Caroline
dc.contributor.authorStaedel, Cathy
dc.contributor.authorIzotte, Julien
dc.contributor.authorSifre, Elodie
dc.contributor.authorLaur, Amandine M
dc.contributor.authorGiese, Alban
dc.contributor.authorKorolik, Victoria
dc.contributor.authorDubus, Pierre
dc.contributor.authorMegraud, Francis
dc.contributor.authorLehours, Philippe
dc.date.accessioned2017-12-06T23:50:20Z
dc.date.available2017-12-06T23:50:20Z
dc.date.issued2017
dc.identifier.issn2235-2988
dc.identifier.doi10.3389/fcimb.2017.00185
dc.identifier.urihttp://hdl.handle.net/10072/353426
dc.description.abstractHelicobacter pylori infection is considered as an excellent model of chronic inflammation-induced tumor development. Our project focuses on gastric MALT lymphoma (GML) related to H. pylori infection and mediated by the chronic inflammatory process initiated by the infection. Recently, microRNAs (miRNAs) have emerged as a new class of gene regulators, which play key roles in inflammation and carcinogenesis acting as oncogenes or tumor suppressors. Their precise characterization in the development of inflammation and their contribution in regulating host cells responses to infection by H. pylori have been little explored. Our goal was to analyze the changes in miRNAs in a GML mouse model using BALB/c mice thymectomized at day 3 post-birth (d3Tx model) and to clarify their implication in GML pathogenesis. PCR array followed by RT-qPCR identified five miRNAs (miR-21a, miR-135b, miR-142a, miR-150, miR-155) overexpressed in the stomachs of GML-developing d3Tx mice infected by H. pylori. The analysis of their putative targets allowed us to identify TP53INP1, an anti-proliferative and pro-apoptotic protein, as a common target of 4 of the 5 up-regulated miRNAs. We postulate that these miRNAs may act in synergy to promote the development of GML. miR-142a was also overexpressed in mouse sera samples and therefore could serve as a diagnostic marker. In situ hybridization on gastric samples with miR-142a revealed a global up-regulation of this miRNA by the tumor microenvironment at the lymphoma stage. Dysregulation of miR-21a, miR-135b, miR-142a, miR-150, miR-155 could play a critical role in the pathogenesis of GML and might offer potential applications as therapeutic targets and novel biomarkers for this disease.
dc.description.peerreviewedYes
dc.languageEnglish
dc.language.isoeng
dc.publisherFrontiers Research Foundation
dc.relation.ispartofpagefrom185-1
dc.relation.ispartofpageto185-11
dc.relation.ispartofjournalFrontiers in Cellular and Infection Microbiology
dc.relation.ispartofvolume7
dc.subject.fieldofresearchMicrobiology not elsewhere classified
dc.subject.fieldofresearchBiochemistry and Cell Biology
dc.subject.fieldofresearchMicrobiology
dc.subject.fieldofresearchcode060599
dc.subject.fieldofresearchcode0601
dc.subject.fieldofresearchcode0605
dc.titleDeregulation of MicroRNAs in Gastric Lymphomagenesis Induced in the d3Tx Mouse Model of Helicobacter pylori Infection
dc.typeJournal article
dc.type.descriptionC1 - Articles
dc.type.codeC - Journal Articles
dcterms.licensehttps://creativecommons.org/licenses/by/4.0/
dc.description.versionVersion of Record (VoR)
gro.rights.copyright© 2017 Floch, Capdevielle, Staedel, Izotte, Sifré, Laur, Giese, Korolik, Dubus, Mégraud and Lehours. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
gro.hasfulltextFull Text
gro.griffith.authorKorolik, Victoria


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