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MiR-10a and HOXB4 are overexpressed in atypical myeloproliferative neoplasms

hal.structure.identifierCHU Bordeaux
hal.structure.identifierBiothérapies des maladies génétiques et cancers
dc.contributor.authorDUMAS, Pierre-Yves
hal.structure.identifierLaboratoire d'hématologie
hal.structure.identifierActions for OnCogenesis understanding and Target Identification in ONcology [ACTION]
dc.contributor.authorMANSIER, Olivier
hal.structure.identifierActions for OnCogenesis understanding and Target Identification in ONcology [ACTION]
dc.contributor.authorPROUZET-MAULÉON, Valérie
hal.structure.identifierThe University of Tokyo [UTokyo]
dc.contributor.authorKOYA, Junji
hal.structure.identifierInstitut National de la Santé et de la Recherche Médicale [INSERM]
dc.contributor.authorVILLACRECES, Arnaud
hal.structure.identifierEtablissement Français du Sang
dc.contributor.authorBRUNET DE LA GRANGE, Philippe
hal.structure.identifierLaboratoire d'hématologie
dc.contributor.authorLUQUE PAZ, Damien
hal.structure.identifierLaboratoire d'hématologie
dc.contributor.authorBIDET, Audrey
hal.structure.identifierBiothérapies des maladies génétiques et cancers
dc.contributor.authorPASQUET, Jean-Max
hal.structure.identifierLaboratoire d'hématologie
hal.structure.identifierBiothérapies des maladies génétiques et cancers
dc.contributor.authorPRALORAN, Vincent
hal.structure.identifierBiodiversité, Gènes & Communautés [BioGeCo]
dc.contributor.authorSALIN, Franck
hal.structure.identifierThe University of Tokyo [UTokyo]
dc.contributor.authorKUROKAWA, Mineo
hal.structure.identifierActions for OnCogenesis understanding and Target Identification in ONcology [ACTION]
hal.structure.identifierInstitut Bergonié [Bordeaux]
dc.contributor.authorMAHON, François-Xavier
hal.structure.identifierActions for OnCogenesis understanding and Target Identification in ONcology [ACTION]
hal.structure.identifierInstitut National Polytechnique
dc.contributor.authorCARDINAUD, Bruno
hal.structure.identifierLaboratoire d'hématologie
hal.structure.identifierBiothérapies des maladies génétiques et cancers
hal.structure.identifierService d'hématologie biologique
hal.structure.identifierGénétique, génomique fonctionnelle et biotechnologies (UMR 1078) [GGB]
dc.contributor.authorLIPPERT, Eric
dc.date.issued2018
dc.identifier.issn1471-2407
dc.description.abstractEn<strong>Background</strong> Atypical Myeloproliferative Neoplasms (aMPN) share characteristics of MPN and Myelodysplastic Syndromes. Although abnormalities in cytokine signaling are common in MPN, the pathophysiology of atypical MPN still remains elusive. Since deregulation of microRNAs is involved in the biology of various cancers, we studied the miRNome of aMPN patients. <strong>Methods</strong> MiRNome and mutations in epigenetic regulator genes ASXL1, TET2, DNMT3A, EZH2 and IDH1/2 were explored in aMPN patients. Epigenetic regulation of miR-10a and HOXB4 expression was investigated by treating hematopoietic cell lines with 5-aza-2’deoxycytidine, valproic acid and retinoic acid. Functional effects of miR-10a overexpression on cell proliferation, differentiation and self-renewal were studied by transducing CD34+ cells with lentiviral vectors encoding the pri-miR-10a precursor. <strong>Results</strong> MiR-10a was identified as the most significantly up-regulated microRNA in aMPN. MiR-10a expression correlated with that of HOXB4, sitting in the same genomic locus. The transcription of these two genes was increased by DNA demethylation and histone acetylation, both necessary for optimal expression induction by retinoic acid. Moreover, miR-10a and HOXB4 overexpression seemed associated with DNMT3A mutation in hematological malignancies. However, overexpression of miR-10a had no effect on proliferation, differentiation or self-renewal of normal hematopoietic progenitors. <strong>Conclusions</strong> MiR-10a and HOXB4 are overexpressed in aMPN. This overexpression seems to be the result of abnormalities in epigenetic regulation mechanisms. Our data suggest that miR-10a could represent a simple marker of transcription at this genomic locus including HOXB4, widely recognized as involved in stem cell expansion.
dc.language.isoen
dc.publisherBioMed Central
dc.rights.urihttp://creativecommons.org/licenses/by/
dc.subjectmiR-10a
dc.subject.enDNMT3A
dc.subject.enHOXB4
dc.subject.enatypical myeloproliferative neoplasms
dc.subject.enepigenetic
dc.title.enMiR-10a and HOXB4 are overexpressed in atypical myeloproliferative neoplasms
dc.typeArticle de revue
dc.identifier.doi10.1186/s12885-018-4993-2
dc.subject.halSciences du Vivant [q-bio]
bordeaux.journalBMC Cancer
bordeaux.page1-11
bordeaux.volume18
bordeaux.issue1
bordeaux.peerReviewedoui
hal.identifierhal-02622723
hal.version1
hal.popularnon
hal.audienceInternationale
hal.origin.linkhttps://hal.archives-ouvertes.fr//hal-02622723v1
bordeaux.COinSctx_ver=Z39.88-2004&amp;rft_val_fmt=info:ofi/fmt:kev:mtx:journal&amp;rft.jtitle=BMC%20Cancer&amp;rft.date=2018&amp;rft.volume=18&amp;rft.issue=1&amp;rft.spage=1-11&amp;rft.epage=1-11&amp;rft.eissn=1471-2407&amp;rft.issn=1471-2407&amp;rft.au=DUMAS,%20Pierre-Yves&amp;MANSIER,%20Olivier&amp;PROUZET-MAUL%C3%89ON,%20Val%C3%A9rie&amp;KOYA,%20Junji&amp;VILLACRECES,%20Arnaud&amp;rft.genre=article


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