Article: Dysregulated microRNAs affect pathways and targets of biologic relevance in nasal-type natural killer/T-cell lymphoma
| Title | Dysregulated microRNAs affect pathways and targets of biologic relevance in nasal-type natural killer/T-cell lymphoma |
|---|---|
| Authors | Ng, SB1 Yan, J4 Huang, G4 Selvarajan, V1 Tay, JLS4 Lin, B4 Bi, C4 Tan, J4 Kwong, YL2 Shimizu, N5 Aozasa, K3 Chng, WJ4 6 |
| Issue Date | 2011 |
| Publisher | American 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?] DOI: http://dx.doi.org/10.1182/blood-2011-07-364224 |
| 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 ∇ 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. |
| ISSN | 0006-4971 2011 Impact Factor: 9.898 2011 SCImago Journal Rankings: 1.698 |
| DOI | http://dx.doi.org/10.1182/blood-2011-07-364224 |
| References | References in Scopus |
| dc.contributor.author | Ng, SB |
|---|---|
| dc.contributor.author | Yan, J |
| dc.contributor.author | Huang, G |
| dc.contributor.author | Selvarajan, V |
| dc.contributor.author | Tay, JLS |
| dc.contributor.author | Lin, B |
| dc.contributor.author | Bi, C |
| dc.contributor.author | Tan, J |
| dc.contributor.author | Kwong, YL |
| dc.contributor.author | Shimizu, N |
| dc.contributor.author | Aozasa, K |
| dc.contributor.author | Chng, WJ |
| dc.date.accessioned | 2012-09-05T05:31:05Z |
| dc.date.available | 2012-09-05T05:31:05Z |
| dc.date.issued | 2011 |
| dc.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 ∇ 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.nature | Link_to_subscribed_fulltext |
| dc.identifier.citation | Blood, 2011, v. 118 n. 18, p. 4919-4929 [How to Cite?] DOI: http://dx.doi.org/10.1182/blood-2011-07-364224 |
| dc.identifier.citeulike | 10001569 |
| dc.identifier.doi | http://dx.doi.org/10.1182/blood-2011-07-364224 |
| dc.identifier.epage | 4929 |
| dc.identifier.issn | 0006-4971 2011 Impact Factor: 9.898 2011 SCImago Journal Rankings: 1.698 |
| dc.identifier.issue | 18 |
| dc.identifier.pmid | 21921041 |
| dc.identifier.scopus | eid_2-s2.0-80855128777 |
| dc.identifier.spage | 4919 |
| dc.identifier.uri | http://hdl.handle.net/10722/163413 |
| dc.identifier.volume | 118 |
| dc.language | eng |
| dc.publisher | American Society of Hematology. The Journal's web site is located at http://bloodjournal.hematologylibrary.org/ |
| dc.publisher.place | United States |
| dc.relation.ispartof | Blood |
| dc.relation.references | References in Scopus |
| dc.subject.mesh | Animals |
| dc.subject.mesh | Caenorhabditis Elegans - Genetics |
| dc.subject.mesh | Cell Line, Tumor |
| dc.subject.mesh | Cluster Analysis |
| dc.subject.mesh | Gene Expression Profiling |
| dc.subject.mesh | Gene Expression Regulation, Neoplastic - Physiology |
| dc.subject.mesh | Humans |
| dc.subject.mesh | Killer Cells, Natural - Metabolism - Pathology |
| dc.subject.mesh | Lymphoma, Extranodal Nk-T-Cell - Diagnosis - Genetics - Metabolism - Therapy |
| dc.subject.mesh | Micrornas - Genetics - Metabolism |
| dc.subject.mesh | Microarray Analysis |
| dc.subject.mesh | Molecular Targeted Therapy |
| dc.subject.mesh | Prognosis |
| dc.subject.mesh | Signal Transduction - Genetics - Physiology |
| dc.subject.mesh | Transfection |
| dc.title | Dysregulated microRNAs affect pathways and targets of biologic relevance in nasal-type natural killer/T-cell lymphoma |
| dc.type | Article |
Author Affiliations
- Yong Loo Lin School of Medicine
- Queen Mary Hospital Hong Kong
- Osaka University Faculty of Medicine
- National University of Singapore
- Tokyo Medical and Dental University
- National University Hospital, Singapore

