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Article: Modulation of LMP2A expression by a newly identified Epstein-Barr virus-encoded microRNA miR-BART22

TitleModulation of LMP2A expression by a newly identified Epstein-Barr virus-encoded microRNA miR-BART22
Authors
Issue Date2009
PublisherNeoplasia Press. The Journal's web site is located at http://www.neoplasia.org
Citation
Neoplasia, 2009, v. 11 n. 11, p. 1174-1184 How to Cite?
AbstractInfection with the Epstein-Barr virus (EBV) is a strong predisposing factor in the development of nasopharyngeal carcinoma (NPC). Many viral gene products including EBNA1, LMP1, and LMP2 have been implicated in NPC tumorigenesis, although the de novo control of these viral oncoproteins remains largely unclear. The recent discovery of EBV-encoded viral microRNA (miRNA) in lymphoid malignancies has prompted us to examine the NPC-associated EBV miRNA. Using large-scale cloning analysis on EBV-positive NPC cells, two novel EBV miRNA, now named miRBART21 and miR-BART22, were identified. These two EBV-encoded miRNA are abundantly expressed in most NPC samples. We found two nucleotide variations in the primary transcript of miR-BART22, which we experimentally confirmed to augment its biogenesis in vitro and thus may underline the high and consistent expression of miRBART22 in NPC tumors. More importantly, we determined that the EBV latent membrane protein 2A (LMP2A) is the putative target of miR-BART22. LMP2A is a potent immunogenic viral antigen that is recognized by the cytotoxic T cells; down-modulation of LMP2A expression by miR-BART22 may permit escape of EBV-infected cells from host immune surveillance. Taken together, we demonstrated that two newly identified EBV-encoded miRNA are highly expressed in NPC. Specific sequence variations on the prevalent EBV strain in our locality might contribute to the higher miR-BART22 expression level in our NPC samples. Our findings emphasize the role of miR-BART22 in modulating LMP2A expression, which may facilitate NPC carcinogenesis by evading the host immune response. Copyright © 2009 Neoplasia Press, Inc. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/92377
ISSN
2014 Impact Factor: 4.252
2015 SCImago Journal Rankings: 2.541
PubMed Central ID
ISI Accession Number ID
Funding AgencyGrant Number
Hong Kong Government Research Fund for the Control of Infectious Diseases06060372
07060242
UGC Collaborated Research FundCUHK04/CRF/08
Funding Information:

This research was supported by Hong Kong Government Research Fund for the Control of Infectious Diseases (Project Code 06060372 and 07060242) and in part by UGC Collaborated Research Fund (CUHK04/CRF/08).

References

 

DC FieldValueLanguage
dc.contributor.authorLung, RWMen_HK
dc.contributor.authorTong, JHMen_HK
dc.contributor.authorSung, YMen_HK
dc.contributor.authorLeung, PSen_HK
dc.contributor.authorNg, DCHen_HK
dc.contributor.authorChau, SLen_HK
dc.contributor.authorChan, AWHen_HK
dc.contributor.authorNg, EKOen_HK
dc.contributor.authorLo, KWen_HK
dc.contributor.authorTo, KFen_HK
dc.date.accessioned2010-09-17T10:44:16Z-
dc.date.available2010-09-17T10:44:16Z-
dc.date.issued2009en_HK
dc.identifier.citationNeoplasia, 2009, v. 11 n. 11, p. 1174-1184en_HK
dc.identifier.issn1522-8002en_HK
dc.identifier.urihttp://hdl.handle.net/10722/92377-
dc.description.abstractInfection with the Epstein-Barr virus (EBV) is a strong predisposing factor in the development of nasopharyngeal carcinoma (NPC). Many viral gene products including EBNA1, LMP1, and LMP2 have been implicated in NPC tumorigenesis, although the de novo control of these viral oncoproteins remains largely unclear. The recent discovery of EBV-encoded viral microRNA (miRNA) in lymphoid malignancies has prompted us to examine the NPC-associated EBV miRNA. Using large-scale cloning analysis on EBV-positive NPC cells, two novel EBV miRNA, now named miRBART21 and miR-BART22, were identified. These two EBV-encoded miRNA are abundantly expressed in most NPC samples. We found two nucleotide variations in the primary transcript of miR-BART22, which we experimentally confirmed to augment its biogenesis in vitro and thus may underline the high and consistent expression of miRBART22 in NPC tumors. More importantly, we determined that the EBV latent membrane protein 2A (LMP2A) is the putative target of miR-BART22. LMP2A is a potent immunogenic viral antigen that is recognized by the cytotoxic T cells; down-modulation of LMP2A expression by miR-BART22 may permit escape of EBV-infected cells from host immune surveillance. Taken together, we demonstrated that two newly identified EBV-encoded miRNA are highly expressed in NPC. Specific sequence variations on the prevalent EBV strain in our locality might contribute to the higher miR-BART22 expression level in our NPC samples. Our findings emphasize the role of miR-BART22 in modulating LMP2A expression, which may facilitate NPC carcinogenesis by evading the host immune response. Copyright © 2009 Neoplasia Press, Inc. All rights reserved.en_HK
dc.languageengen_HK
dc.publisherNeoplasia Press. The Journal's web site is located at http://www.neoplasia.orgen_HK
dc.relation.ispartofNeoplasiaen_HK
dc.subject.meshGene Expression Regulation, Viral-
dc.subject.meshHerpesvirus 4, Human - genetics-
dc.subject.meshMicroRNAs - genetics-
dc.subject.meshNasopharyngeal Neoplasms - virology-
dc.subject.meshViral Matrix Proteins - biosynthesis - genetics-
dc.titleModulation of LMP2A expression by a newly identified Epstein-Barr virus-encoded microRNA miR-BART22en_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1522-8002&volume=11&issue=11&spage=1174&epage=1184&date=2009&atitle=Modulation+of+LMP2A+expression+by+a+newly+identified+Epstein-Barr+virus-encoded+microRNA+miR-BART22-
dc.identifier.emailNg, EKO: ngko@hku.hken_HK
dc.identifier.authorityNg, EKO=rp01364en_HK
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1593/neo.09888en_HK
dc.identifier.pmid19881953-
dc.identifier.pmcidPMC2767219-
dc.identifier.scopuseid_2-s2.0-70350724544en_HK
dc.identifier.hkuros168715-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-70350724544&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume11en_HK
dc.identifier.issue11en_HK
dc.identifier.spage1174en_HK
dc.identifier.epage1184en_HK
dc.identifier.isiWOS:000272473900006-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridLung, RWM=22980272500en_HK
dc.identifier.scopusauthoridTong, JHM=7202724564en_HK
dc.identifier.scopusauthoridSung, YM=7201550229en_HK
dc.identifier.scopusauthoridLeung, PS=55085137800en_HK
dc.identifier.scopusauthoridNg, DCH=36151217700en_HK
dc.identifier.scopusauthoridChau, SL=35331875400en_HK
dc.identifier.scopusauthoridChan, AWH=25930306100en_HK
dc.identifier.scopusauthoridNg, EKO=21135553700en_HK
dc.identifier.scopusauthoridLo, KW=7402101603en_HK
dc.identifier.scopusauthoridTo, KF=24336843300en_HK

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