Deregulation of MicroRNAs in Gastric Lymphomagenesis Induced in the d3Tx Mouse Model of Helicobacter pylori Infection.
Identifieur interne : 000C66 ( PubMed/Curation ); précédent : 000C65; suivant : 000C67Deregulation of MicroRNAs in Gastric Lymphomagenesis Induced in the d3Tx Mouse Model of Helicobacter pylori Infection.
Auteurs : Pauline Floch [France] ; Caroline Capdevielle [France] ; Cathy Staedel [France] ; Julien Izotte [France] ; Elodie Sifré [France] ; Amandine M. Laur [France] ; Alban Giese [France] ; Victoria Korolik [Australie] ; Pierre Dubus [France] ; Francis Mégraud [France] ; Philippe Lehours [France]Source :
- Frontiers in cellular and infection microbiology [ 2235-2988 ] ; 2017.
Abstract
Helicobacter 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.
DOI: 10.3389/fcimb.2017.00185
PubMed: 28560185
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Infection.</title><author><name sortKey="Floch, Pauline" sort="Floch, Pauline" uniqKey="Floch P" first="Pauline" last="Floch">Pauline Floch</name><affiliation wicri:level="1"><nlm:affiliation>UMR1053 Bordeaux Research in Translational Oncology, Institut National de la Santé et de la Recherche Médicale, University of BordeauxBordeaux, France.</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>UMR1053 Bordeaux Research in Translational Oncology, Institut National de la Santé et de la Recherche Médicale, University of BordeauxBordeaux</wicri:regionArea></affiliation></author><author><name sortKey="Capdevielle, Caroline" sort="Capdevielle, Caroline" uniqKey="Capdevielle C" first="Caroline" last="Capdevielle">Caroline Capdevielle</name><affiliation wicri:level="1"><nlm:affiliation>UMR1053 Bordeaux Research in Translational Oncology, Institut National de la Santé et de la Recherche Médicale, University of BordeauxBordeaux, France.</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>UMR1053 Bordeaux Research in Translational Oncology, Institut National de la Santé et de la Recherche Médicale, University of BordeauxBordeaux</wicri:regionArea></affiliation></author><author><name sortKey="Staedel, Cathy" sort="Staedel, Cathy" uniqKey="Staedel C" first="Cathy" last="Staedel">Cathy Staedel</name><affiliation wicri:level="1"><nlm:affiliation>ARNA Laboratory, Institut National de la Santé et de la Recherche Médicale U1212, Université de BordeauxBordeaux, France.</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>ARNA Laboratory, Institut National de la Santé et de la Recherche Médicale U1212, Université de BordeauxBordeaux</wicri:regionArea></affiliation></author><author><name sortKey="Izotte, Julien" sort="Izotte, Julien" uniqKey="Izotte J" first="Julien" last="Izotte">Julien Izotte</name><affiliation wicri:level="1"><nlm:affiliation>UMR1053 Bordeaux Research in Translational Oncology, Institut National de la Santé et de la Recherche Médicale, University of BordeauxBordeaux, France.</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>UMR1053 Bordeaux Research in Translational Oncology, Institut National de la Santé et de la Recherche Médicale, University of BordeauxBordeaux</wicri:regionArea></affiliation></author><author><name sortKey="Sifre, Elodie" sort="Sifre, Elodie" uniqKey="Sifre E" first="Elodie" last="Sifré">Elodie Sifré</name><affiliation wicri:level="1"><nlm:affiliation>UMR1053 Bordeaux Research in Translational Oncology, Institut National de la Santé et de la Recherche Médicale, University of BordeauxBordeaux, France.</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>UMR1053 Bordeaux Research in Translational Oncology, Institut National de la Santé et de la Recherche Médicale, University of BordeauxBordeaux</wicri:regionArea></affiliation></author><author><name sortKey="Laur, Amandine M" sort="Laur, Amandine M" uniqKey="Laur A" first="Amandine M" last="Laur">Amandine M. Laur</name><affiliation wicri:level="1"><nlm:affiliation>UMR1053 Bordeaux Research in Translational Oncology, Institut National de la Santé et de la Recherche Médicale, University of BordeauxBordeaux, France.</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>UMR1053 Bordeaux Research in Translational Oncology, Institut National de la Santé et de la Recherche Médicale, University of BordeauxBordeaux</wicri:regionArea></affiliation></author><author><name sortKey="Giese, Alban" sort="Giese, Alban" uniqKey="Giese A" first="Alban" last="Giese">Alban Giese</name><affiliation wicri:level="1"><nlm:affiliation>UMR1053 Bordeaux Research in Translational Oncology, Institut National de la Santé et de la Recherche Médicale, University of BordeauxBordeaux, France.</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>UMR1053 Bordeaux Research in Translational Oncology, Institut National de la Santé et de la Recherche Médicale, University of BordeauxBordeaux</wicri:regionArea></affiliation></author><author><name sortKey="Korolik, Victoria" sort="Korolik, Victoria" uniqKey="Korolik V" first="Victoria" last="Korolik">Victoria Korolik</name><affiliation wicri:level="1"><nlm:affiliation>Institute for Glycomics, Griffith UniversityGold Coast, QLD, Australia.</nlm:affiliation><country xml:lang="fr">Australie</country><wicri:regionArea>Institute for Glycomics, Griffith UniversityGold Coast, QLD</wicri:regionArea></affiliation></author><author><name sortKey="Dubus, Pierre" sort="Dubus, Pierre" uniqKey="Dubus P" first="Pierre" last="Dubus">Pierre Dubus</name><affiliation wicri:level="1"><nlm:affiliation>UMR1053 Bordeaux Research in Translational Oncology, Institut National de la Santé et de la Recherche Médicale, University of BordeauxBordeaux, France.</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>UMR1053 Bordeaux Research in Translational Oncology, Institut National de la Santé et de la Recherche Médicale, University of BordeauxBordeaux</wicri:regionArea></affiliation></author><author><name sortKey="Megraud, Francis" sort="Megraud, Francis" uniqKey="Megraud F" first="Francis" last="Mégraud">Francis Mégraud</name><affiliation wicri:level="1"><nlm:affiliation>UMR1053 Bordeaux Research in Translational Oncology, Institut National de la Santé et de la Recherche Médicale, University of BordeauxBordeaux, France.</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>UMR1053 Bordeaux Research in Translational Oncology, Institut National de la Santé et de la Recherche Médicale, University of BordeauxBordeaux</wicri:regionArea></affiliation></author><author><name sortKey="Lehours, Philippe" sort="Lehours, Philippe" uniqKey="Lehours P" first="Philippe" last="Lehours">Philippe Lehours</name><affiliation wicri:level="1"><nlm:affiliation>UMR1053 Bordeaux Research in Translational Oncology, Institut National de la Santé et de la Recherche Médicale, University of BordeauxBordeaux, France.</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>UMR1053 Bordeaux Research in Translational Oncology, Institut National de la Santé et de la Recherche Médicale, University of BordeauxBordeaux</wicri:regionArea></affiliation></author></analytic><series><title level="j">Frontiers in cellular and infection microbiology</title><idno type="eISSN">2235-2988</idno><imprint><date when="2017" type="published">2017</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Helicobacter 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.</div></front></TEI><pubmed><MedlineCitation Status="In-Process" Owner="NLM"><PMID Version="1">28560185</PMID><DateCreated><Year>2017</Year><Month>05</Month><Day>31</Day></DateCreated><DateRevised><Year>2017</Year><Month>06</Month><Day>06</Day></DateRevised><Article PubModel="Electronic-eCollection"><Journal><ISSN IssnType="Electronic">2235-2988</ISSN><JournalIssue CitedMedium="Internet"><Volume>7</Volume><PubDate><Year>2017</Year></PubDate></JournalIssue><Title>Frontiers in cellular and infection microbiology</Title><ISOAbbreviation>Front Cell Infect Microbiol</ISOAbbreviation></Journal><ArticleTitle>Deregulation of MicroRNAs in Gastric Lymphomagenesis Induced in the d3Tx Mouse Model of Helicobacter pylori Infection.</ArticleTitle><Pagination><MedlinePgn>185</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.3389/fcimb.2017.00185</ELocationID><Abstract><AbstractText>Helicobacter 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.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Floch</LastName><ForeName>Pauline</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>UMR1053 Bordeaux Research in Translational Oncology, Institut National de la Santé et de la Recherche Médicale, University of BordeauxBordeaux, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Capdevielle</LastName><ForeName>Caroline</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>UMR1053 Bordeaux Research in Translational Oncology, Institut National de la Santé et de la Recherche Médicale, University of BordeauxBordeaux, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Staedel</LastName><ForeName>Cathy</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>ARNA Laboratory, Institut National de la Santé et de la Recherche Médicale U1212, Université de BordeauxBordeaux, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Izotte</LastName><ForeName>Julien</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>UMR1053 Bordeaux Research in Translational Oncology, Institut National de la Santé et de la Recherche Médicale, University of BordeauxBordeaux, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sifré</LastName><ForeName>Elodie</ForeName><Initials>E</Initials><AffiliationInfo><Affiliation>UMR1053 Bordeaux Research in Translational Oncology, Institut National de la Santé et de la Recherche Médicale, University of BordeauxBordeaux, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Laur</LastName><ForeName>Amandine M</ForeName><Initials>AM</Initials><AffiliationInfo><Affiliation>UMR1053 Bordeaux Research in Translational Oncology, Institut National de la Santé et de la Recherche Médicale, University of BordeauxBordeaux, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Giese</LastName><ForeName>Alban</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>UMR1053 Bordeaux Research in Translational Oncology, Institut National de la Santé et de la Recherche Médicale, University of BordeauxBordeaux, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Korolik</LastName><ForeName>Victoria</ForeName><Initials>V</Initials><AffiliationInfo><Affiliation>Institute for Glycomics, Griffith UniversityGold Coast, QLD, Australia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Dubus</LastName><ForeName>Pierre</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>UMR1053 Bordeaux Research in Translational Oncology, Institut National de la Santé et de la Recherche Médicale, University of BordeauxBordeaux, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Mégraud</LastName><ForeName>Francis</ForeName><Initials>F</Initials><AffiliationInfo><Affiliation>UMR1053 Bordeaux Research in Translational Oncology, Institut National de la Santé et de la Recherche Médicale, University of BordeauxBordeaux, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lehours</LastName><ForeName>Philippe</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>UMR1053 Bordeaux Research in Translational Oncology, Institut National de la Santé et de la Recherche Médicale, University of BordeauxBordeaux, France.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate 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RefType="Cites"><RefSource>Saudi J Gastroenterol. 2016 Jan-Feb;22(1):30-6</RefSource><PMID Version="1">26831604</PMID></CommentsCorrections></CommentsCorrectionsList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Helicobacter pylori</Keyword><Keyword MajorTopicYN="N">MALT lymphoma</Keyword><Keyword MajorTopicYN="N">TP53INP1</Keyword><Keyword MajorTopicYN="N">apoptosis</Keyword><Keyword MajorTopicYN="N">microRNAs</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2017</Year><Month>02</Month><Day>28</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2017</Year><Month>04</Month><Day>27</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2017</Year><Month>6</Month><Day>1</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2017</Year><Month>6</Month><Day>1</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate 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