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Article: Dysregulated microRNAs affect pathways and targets of biologic relevance in nasal-type natural killer/T-cell lymphoma
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TitleDysregulated microRNAs affect pathways and targets of biologic relevance in nasal-type natural killer/T-cell lymphoma
 
AuthorsNg, SB1
Yan, J4
Huang, G4
Selvarajan, V1
Tay, JLS1
Lin, B4
Bi, C4
Tan, J1
Kwong, YL2
Shimizu, N3
Aozasa, K5
Chng, WJ6 4 1
 
Issue Date2011
 
PublisherAmerican Society of Hematology. The Journal's web site is located at http://bloodjournal.hematologylibrary.org/
 
CitationBlood, 2011, v. 118 n. 18, p. 4919-4929 [How to Cite?]
DOI: http://dx.doi.org/10.1182/blood-2011-07-364224
 
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.
 
ISSN0006-4971
2013 Impact Factor: 9.775
 
DOIhttp://dx.doi.org/10.1182/blood-2011-07-364224
 
ReferencesReferences in Scopus
 
DC FieldValue
dc.contributor.authorNg, SB
 
dc.contributor.authorYan, J
 
dc.contributor.authorHuang, G
 
dc.contributor.authorSelvarajan, V
 
dc.contributor.authorTay, JLS
 
dc.contributor.authorLin, B
 
dc.contributor.authorBi, C
 
dc.contributor.authorTan, J
 
dc.contributor.authorKwong, YL
 
dc.contributor.authorShimizu, N
 
dc.contributor.authorAozasa, K
 
dc.contributor.authorChng, WJ
 
dc.date.accessioned2012-09-05T05:31:05Z
 
dc.date.available2012-09-05T05:31:05Z
 
dc.date.issued2011
 
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.
 
dc.description.naturelink_to_subscribed_fulltext
 
dc.identifier.citationBlood, 2011, v. 118 n. 18, p. 4919-4929 [How to Cite?]
DOI: http://dx.doi.org/10.1182/blood-2011-07-364224
 
dc.identifier.citeulike10001569
 
dc.identifier.doihttp://dx.doi.org/10.1182/blood-2011-07-364224
 
dc.identifier.epage4929
 
dc.identifier.issn0006-4971
2013 Impact Factor: 9.775
 
dc.identifier.issue18
 
dc.identifier.pmid21921041
 
dc.identifier.scopuseid_2-s2.0-80855128777
 
dc.identifier.spage4919
 
dc.identifier.urihttp://hdl.handle.net/10722/163413
 
dc.identifier.volume118
 
dc.languageeng
 
dc.publisherAmerican Society of Hematology. The Journal's web site is located at http://bloodjournal.hematologylibrary.org/
 
dc.publisher.placeUnited States
 
dc.relation.ispartofBlood
 
dc.relation.referencesReferences in Scopus
 
dc.subject.meshAnimals
 
dc.subject.meshCaenorhabditis Elegans - Genetics
 
dc.subject.meshCell Line, Tumor
 
dc.subject.meshCluster Analysis
 
dc.subject.meshGene Expression Profiling
 
dc.subject.meshGene Expression Regulation, Neoplastic - Physiology
 
dc.subject.meshHumans
 
dc.subject.meshKiller Cells, Natural - Metabolism - Pathology
 
dc.subject.meshLymphoma, Extranodal Nk-T-Cell - Diagnosis - Genetics - Metabolism - Therapy
 
dc.subject.meshMicrornas - Genetics - Metabolism
 
dc.subject.meshMicroarray Analysis
 
dc.subject.meshMolecular Targeted Therapy
 
dc.subject.meshPrognosis
 
dc.subject.meshSignal Transduction - Genetics - Physiology
 
dc.subject.meshTransfection
 
dc.titleDysregulated microRNAs affect pathways and targets of biologic relevance in nasal-type natural killer/T-cell lymphoma
 
dc.typeArticle
 
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<contributor.author>Huang, G</contributor.author>
<contributor.author>Selvarajan, V</contributor.author>
<contributor.author>Tay, JLS</contributor.author>
<contributor.author>Lin, B</contributor.author>
<contributor.author>Bi, C</contributor.author>
<contributor.author>Tan, J</contributor.author>
<contributor.author>Kwong, YL</contributor.author>
<contributor.author>Shimizu, N</contributor.author>
<contributor.author>Aozasa, K</contributor.author>
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<description.abstract>We performed a comprehensive genomewide miRNA expression profiling of extranodal nasal-type natural killer/T-cell lymphoma (NKTL) using formalin-fixed paraffin-embedded tissue (n &#8711; 30) and NK cell lines (n &#8711; 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. &#169; 2011 by The American Society of Hematology.</description.abstract>
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<subject.mesh>Humans</subject.mesh>
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<subject.mesh>Lymphoma, Extranodal Nk-T-Cell - Diagnosis - Genetics - Metabolism - Therapy</subject.mesh>
<subject.mesh>Micrornas - Genetics - Metabolism</subject.mesh>
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Author Affiliations
  1. Yong Loo Lin School of Medicine
  2. Queen Mary Hospital Hong Kong
  3. Tokyo Medical and Dental University
  4. National University of Singapore
  5. Osaka University Faculty of Medicine
  6. National University Hospital, Singapore