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Article: Phenotypic alterations induced by the Hong Kong-prevalent Epstein-Barr virus-encoded LMP1 variant (2117-LMP1) in nasopharyngeal epithelial cells

TitlePhenotypic alterations induced by the Hong Kong-prevalent Epstein-Barr virus-encoded LMP1 variant (2117-LMP1) in nasopharyngeal epithelial cells
Authors
Issue Date2004
PublisherJohn Wiley & Sons, Inc.. The Journal's web site is located at http://www3.interscience.wiley.com/journal/29331/home
Citation
International Journal Of Cancer, 2004, v. 109 n. 6, p. 919-925 How to Cite?
Abstract
Epstein-Barr virus (EBV) is closely associated with nasopharyngeal carcinoma (NPC), a common cancer in Hong Kong. The EBV-encoded LMP1 protein is believed to play an important role in cell transformation. We have previously identified a prevalent LMP1 variant (2117-LMP1) that is expressed in 86% of primary NPC in Hong Kong. In this study, the biologic phenotypes induced by 2117-LMP1 were compared with those of the prototypic B95.8-LMP1 in an immortalized nasopharyngeal epithelial cell line, NP69. The 2117-LMP1 could induce cell proliferation and resistance to apoptosis induced by growth factor deprivation. Expression of 2117-LMP1 also suppressed expression of p16, p21 and Bax but induced expression of CDK2 and A20. Compared with B95.8-LMP1, 2117-LMP1 could induce a higher migration ability in NP69 cells but was less efficient in inducing morphologic changes, anchorage-independent growth and cell invasion. Relatively weaker ability of 2117-LMP1 than B95.8-LMP1 in upregulation of vimentin, VEGF and MMP9 as well as in downregulation of E-cadherin was observed. 2117-LMP1 could activate higher level of NF-κB activity in HEK 293 cells than B95.8-LMP1. The present study supports a role of 2117-LMP1 in NPC development by enhancing cell proliferation, cell death inhibition and migration in premalignant nasopharyngeal epithelial cells. Furthermore, our study reveals significant functional differences between 2117-LMP1 and the prototypic B95.8-LMP1. Our results provide insights into the pathologic significance of this prevalent LMP1 variant, 2117-LMP1, in the development of NPC in the Hong Kong population. © 2004 Wiley-Liss, Inc.
Persistent Identifierhttp://hdl.handle.net/10722/149642
ISSN
2013 Impact Factor: 5.007
ISI Accession Number ID
References

 

Author Affiliations
  1. The University of Hong Kong
  2. Prince of Wales Hospital Hong Kong
DC FieldValueLanguage
dc.contributor.authorLo, AKFen_US
dc.contributor.authorHuang, DPen_US
dc.contributor.authorLo, KWen_US
dc.contributor.authorChui, YLen_US
dc.contributor.authorLi, HMen_US
dc.contributor.authorPang, JCSen_US
dc.contributor.authorTsao, SWen_US
dc.date.accessioned2012-06-26T05:56:25Z-
dc.date.available2012-06-26T05:56:25Z-
dc.date.issued2004en_US
dc.identifier.citationInternational Journal Of Cancer, 2004, v. 109 n. 6, p. 919-925en_US
dc.identifier.issn0020-7136en_US
dc.identifier.urihttp://hdl.handle.net/10722/149642-
dc.description.abstractEpstein-Barr virus (EBV) is closely associated with nasopharyngeal carcinoma (NPC), a common cancer in Hong Kong. The EBV-encoded LMP1 protein is believed to play an important role in cell transformation. We have previously identified a prevalent LMP1 variant (2117-LMP1) that is expressed in 86% of primary NPC in Hong Kong. In this study, the biologic phenotypes induced by 2117-LMP1 were compared with those of the prototypic B95.8-LMP1 in an immortalized nasopharyngeal epithelial cell line, NP69. The 2117-LMP1 could induce cell proliferation and resistance to apoptosis induced by growth factor deprivation. Expression of 2117-LMP1 also suppressed expression of p16, p21 and Bax but induced expression of CDK2 and A20. Compared with B95.8-LMP1, 2117-LMP1 could induce a higher migration ability in NP69 cells but was less efficient in inducing morphologic changes, anchorage-independent growth and cell invasion. Relatively weaker ability of 2117-LMP1 than B95.8-LMP1 in upregulation of vimentin, VEGF and MMP9 as well as in downregulation of E-cadherin was observed. 2117-LMP1 could activate higher level of NF-κB activity in HEK 293 cells than B95.8-LMP1. The present study supports a role of 2117-LMP1 in NPC development by enhancing cell proliferation, cell death inhibition and migration in premalignant nasopharyngeal epithelial cells. Furthermore, our study reveals significant functional differences between 2117-LMP1 and the prototypic B95.8-LMP1. Our results provide insights into the pathologic significance of this prevalent LMP1 variant, 2117-LMP1, in the development of NPC in the Hong Kong population. © 2004 Wiley-Liss, Inc.en_US
dc.languageengen_US
dc.publisherJohn Wiley & Sons, Inc.. The Journal's web site is located at http://www3.interscience.wiley.com/journal/29331/homeen_US
dc.relation.ispartofInternational Journal of Canceren_US
dc.subject.meshCdc2-Cdc28 Kinases - Metabolismen_US
dc.subject.meshCadherins - Metabolismen_US
dc.subject.meshCell Divisionen_US
dc.subject.meshCell Movementen_US
dc.subject.meshCell Survivalen_US
dc.subject.meshCyclin-Dependent Kinase 2en_US
dc.subject.meshCyclin-Dependent Kinase Inhibitor P16 - Metabolismen_US
dc.subject.meshCyclin-Dependent Kinase Inhibitor P21en_US
dc.subject.meshCyclins - Metabolismen_US
dc.subject.meshHerpesvirus 4, Human - Physiologyen_US
dc.subject.meshHong Kongen_US
dc.subject.meshHumansen_US
dc.subject.meshIntracellular Signaling Peptides And Proteinsen_US
dc.subject.meshMatrix Metalloproteinase 9 - Metabolismen_US
dc.subject.meshNf-Kappa B - Metabolismen_US
dc.subject.meshNasopharyngeal Neoplasms - Metabolism - Pathology - Virologyen_US
dc.subject.meshNuclear Proteinsen_US
dc.subject.meshPhenotypeen_US
dc.subject.meshProteins - Metabolismen_US
dc.subject.meshProto-Oncogene Proteins - Metabolismen_US
dc.subject.meshProto-Oncogene Proteins C-Bcl-2en_US
dc.subject.meshTumor Cells, Cultureden_US
dc.subject.meshUp-Regulationen_US
dc.subject.meshVascular Endothelial Growth Factor A - Metabolismen_US
dc.subject.meshViral Matrix Proteins - Physiologyen_US
dc.subject.meshBcl-2-Associated X Proteinen_US
dc.titlePhenotypic alterations induced by the Hong Kong-prevalent Epstein-Barr virus-encoded LMP1 variant (2117-LMP1) in nasopharyngeal epithelial cellsen_US
dc.typeArticleen_US
dc.identifier.emailTsao, SW:gswtsao@hkucc.hku.hken_US
dc.identifier.authorityTsao, SW=rp00399en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1002/ijc.20051en_US
dc.identifier.pmid15027126en_US
dc.identifier.scopuseid_2-s2.0-2442486341en_US
dc.identifier.hkuros86248-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-2442486341&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume109en_US
dc.identifier.issue6en_US
dc.identifier.spage919en_US
dc.identifier.epage925en_US
dc.identifier.isiWOS:000220779200015-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridLo, AKF=7102780657en_US
dc.identifier.scopusauthoridHuang, DP=7403891486en_US
dc.identifier.scopusauthoridLo, KW=34872774800en_US
dc.identifier.scopusauthoridChui, YL=7004982375en_US
dc.identifier.scopusauthoridLi, HM=8312261000en_US
dc.identifier.scopusauthoridPang, JCS=7201733981en_US
dc.identifier.scopusauthoridTsao, SW=7102813116en_US

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