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Article: Dysregulated microRNAs affect pathways and targets of biologic relevance in nasal-type natural killer/T-cell lymphoma

TitleDysregulated microRNAs affect pathways and targets of biologic relevance in nasal-type natural killer/T-cell lymphoma
Authors
Issue Date2011
PublisherAmerican Society of Hematology. The Journal's web site is located at http://bloodjournal.hematologylibrary.org/
Citation
Blood, 2011, v. 118 n. 18, p. 4919-4929 How to Cite?
AbstractWe performed a comprehensive genomewide miRNA expression profiling of extranodal nasal-type natural killer/T-cell lymphoma (NKTL) using formalin-fixed paraffin-embedded tissue (n ∇ 30) and NK cell lines (n ∇ 6) compared with normal NK cells, with the objective of understanding the pathogenetic role of miRNA deregulation in NKTL. Compared with normal NK cells, differentially expressed miRNAs in NKTL are predominantly downregulated. Re-expression of downregulated miRNAs, such as miR-101, miR- 26a, miR26b, miR-28-5, and miR-363, reduced the growth of the NK cell line and modulated the expression of their predicted target genes, suggesting the potential functional role of the deregulated miRNAs in the oncogenesis of NKTL. Taken together, the predicted targets whose expression is inversely correlated with the expression of deregulated miRNA in NKTL are significantly enriched for genes involved in cell cycle-related, p53, and MAPK signaling pathways. We also performed immunohistochemical validation for selected target proteins and found overexpression of MUM1, BLIMP1, and STMN1 in NKTL, and notably, a corresponding increase in MYC expression. Because MYC is known to cause repression of miRNA expression, it is possible that MYC activation in NKTL may contribute to the suppression of the miRNAs regulating MUM1, BLIMP1, and STMN1. © 2011 by The American Society of Hematology.
Persistent Identifierhttp://hdl.handle.net/10722/163413
ISSN
2014 Impact Factor: 10.452
2014 SCImago Journal Rankings: 5.246
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorNg, SBen_US
dc.contributor.authorYan, Jen_US
dc.contributor.authorHuang, Gen_US
dc.contributor.authorSelvarajan, Ven_US
dc.contributor.authorTay, JLSen_US
dc.contributor.authorLin, Ben_US
dc.contributor.authorBi, Cen_US
dc.contributor.authorTan, Jen_US
dc.contributor.authorKwong, YLen_US
dc.contributor.authorShimizu, Nen_US
dc.contributor.authorAozasa, Ken_US
dc.contributor.authorChng, WJen_US
dc.date.accessioned2012-09-05T05:31:05Z-
dc.date.available2012-09-05T05:31:05Z-
dc.date.issued2011en_US
dc.identifier.citationBlood, 2011, v. 118 n. 18, p. 4919-4929en_US
dc.identifier.issn0006-4971en_US
dc.identifier.urihttp://hdl.handle.net/10722/163413-
dc.description.abstractWe performed a comprehensive genomewide miRNA expression profiling of extranodal nasal-type natural killer/T-cell lymphoma (NKTL) using formalin-fixed paraffin-embedded tissue (n ∇ 30) and NK cell lines (n ∇ 6) compared with normal NK cells, with the objective of understanding the pathogenetic role of miRNA deregulation in NKTL. Compared with normal NK cells, differentially expressed miRNAs in NKTL are predominantly downregulated. Re-expression of downregulated miRNAs, such as miR-101, miR- 26a, miR26b, miR-28-5, and miR-363, reduced the growth of the NK cell line and modulated the expression of their predicted target genes, suggesting the potential functional role of the deregulated miRNAs in the oncogenesis of NKTL. Taken together, the predicted targets whose expression is inversely correlated with the expression of deregulated miRNA in NKTL are significantly enriched for genes involved in cell cycle-related, p53, and MAPK signaling pathways. We also performed immunohistochemical validation for selected target proteins and found overexpression of MUM1, BLIMP1, and STMN1 in NKTL, and notably, a corresponding increase in MYC expression. Because MYC is known to cause repression of miRNA expression, it is possible that MYC activation in NKTL may contribute to the suppression of the miRNAs regulating MUM1, BLIMP1, and STMN1. © 2011 by The American Society of Hematology.en_US
dc.languageengen_US
dc.publisherAmerican Society of Hematology. The Journal's web site is located at http://bloodjournal.hematologylibrary.org/en_US
dc.relation.ispartofBlooden_US
dc.subject.meshAnimalsen_US
dc.subject.meshCaenorhabditis Elegans - Geneticsen_US
dc.subject.meshCell Line, Tumoren_US
dc.subject.meshCluster Analysisen_US
dc.subject.meshGene Expression Profilingen_US
dc.subject.meshGene Expression Regulation, Neoplastic - Physiologyen_US
dc.subject.meshHumansen_US
dc.subject.meshKiller Cells, Natural - Metabolism - Pathologyen_US
dc.subject.meshLymphoma, Extranodal Nk-T-Cell - Diagnosis - Genetics - Metabolism - Therapyen_US
dc.subject.meshMicrornas - Genetics - Metabolismen_US
dc.subject.meshMicroarray Analysisen_US
dc.subject.meshMolecular Targeted Therapyen_US
dc.subject.meshPrognosisen_US
dc.subject.meshSignal Transduction - Genetics - Physiologyen_US
dc.subject.meshTransfectionen_US
dc.titleDysregulated microRNAs affect pathways and targets of biologic relevance in nasal-type natural killer/T-cell lymphomaen_US
dc.typeArticleen_US
dc.identifier.emailKwong, YL:ylkwong@hku.hken_US
dc.identifier.authorityKwong, YL=rp00358en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1182/blood-2011-07-364224en_US
dc.identifier.pmid21921041en_US
dc.identifier.scopuseid_2-s2.0-80855128777en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-80855128777&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume118en_US
dc.identifier.issue18en_US
dc.identifier.spage4919en_US
dc.identifier.epage4929en_US
dc.identifier.isiWOS:000296714500021-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridNg, SB=7403358752en_US
dc.identifier.scopusauthoridYan, J=7403729331en_US
dc.identifier.scopusauthoridHuang, G=7403424897en_US
dc.identifier.scopusauthoridSelvarajan, V=37075646500en_US
dc.identifier.scopusauthoridTay, JLS=54413308100en_US
dc.identifier.scopusauthoridLin, B=8325951000en_US
dc.identifier.scopusauthoridBi, C=23466476400en_US
dc.identifier.scopusauthoridTan, J=7402302334en_US
dc.identifier.scopusauthoridKwong, YL=7102818954en_US
dc.identifier.scopusauthoridShimizu, N=7403575308en_US
dc.identifier.scopusauthoridAozasa, K=35381404000en_US
dc.identifier.scopusauthoridChng, WJ=8717348700en_US
dc.identifier.citeulike10001569-

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