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

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TitlePhenotypic alterations induced by the Hong Kong-prevalent Epstein-Barr virus-encoded LMP1 variant (2117-LMP1) in nasopharyngeal epithelial cells
AuthorsLo, AKF2
Huang, DP2
Lo, KW2
Chui, YL2
Li, HM
Pang, JCS2
Tsao, SW1
Issue Date2004
PublisherJohn Wiley & Sons, Inc.. The Journal's web site is located at http://www3.interscience.wiley.com/journal/29331/home
CitationInternational Journal Of Cancer, 2004, v. 109 n. 6, p. 919-925 [How to Cite?]
DOI: http://dx.doi.org/10.1002/ijc.20051
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.
ISSN0020-7136
2011 Impact Factor: 5.444
2011 SCImago Journal Rankings: 0.620
DOIhttp://dx.doi.org/10.1002/ijc.20051
ISI Accession Number IDWOS:000220779200015
ReferencesReferences in Scopus
DC Field
Value
dc.contributor.authorLo, AKF
dc.contributor.authorHuang, DP
dc.contributor.authorLo, KW
dc.contributor.authorChui, YL
dc.contributor.authorLi, HM
dc.contributor.authorPang, JCS
dc.contributor.authorTsao, SW
dc.date.accessioned2012-06-26T05:56:25Z
dc.date.available2012-06-26T05:56:25Z
dc.date.issued2004
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.
dc.description.natureLink_to_subscribed_fulltext
dc.identifier.citationInternational Journal Of Cancer, 2004, v. 109 n. 6, p. 919-925 [How to Cite?]
DOI: http://dx.doi.org/10.1002/ijc.20051
dc.identifier.doihttp://dx.doi.org/10.1002/ijc.20051
dc.identifier.epage925
dc.identifier.hkuros86248
dc.identifier.isiWOS:000220779200015
dc.identifier.issn0020-7136
2011 Impact Factor: 5.444
2011 SCImago Journal Rankings: 0.620
dc.identifier.issue6
dc.identifier.pmid15027126
dc.identifier.scopuseid_2-s2.0-2442486341
dc.identifier.spage919
dc.identifier.urihttp://hdl.handle.net/10722/149642
dc.identifier.volume109
dc.languageeng
dc.publisherJohn Wiley & Sons, Inc.. The Journal's web site is located at http://www3.interscience.wiley.com/journal/29331/home
dc.publisher.placeUnited States
dc.relation.ispartofInternational Journal of Cancer
dc.relation.referencesReferences in Scopus
dc.subject.meshCdc2-Cdc28 Kinases - Metabolism
dc.subject.meshCadherins - Metabolism
dc.subject.meshCell Division
dc.subject.meshCell Movement
dc.subject.meshCell Survival
dc.subject.meshCyclin-Dependent Kinase 2
dc.subject.meshCyclin-Dependent Kinase Inhibitor P16 - Metabolism
dc.subject.meshCyclin-Dependent Kinase Inhibitor P21
dc.subject.meshCyclins - Metabolism
dc.subject.meshHerpesvirus 4, Human - Physiology
dc.subject.meshHong Kong
dc.subject.meshHumans
dc.subject.meshIntracellular Signaling Peptides And Proteins
dc.subject.meshMatrix Metalloproteinase 9 - Metabolism
dc.subject.meshNf-Kappa B - Metabolism
dc.subject.meshNasopharyngeal Neoplasms - Metabolism - Pathology - Virology
dc.subject.meshNuclear Proteins
dc.subject.meshPhenotype
dc.subject.meshProteins - Metabolism
dc.subject.meshProto-Oncogene Proteins - Metabolism
dc.subject.meshProto-Oncogene Proteins C-Bcl-2
dc.subject.meshTumor Cells, Cultured
dc.subject.meshUp-Regulation
dc.subject.meshVascular Endothelial Growth Factor A - Metabolism
dc.subject.meshViral Matrix Proteins - Physiology
dc.subject.meshBcl-2-Associated X Protein
dc.titlePhenotypic alterations induced by the Hong Kong-prevalent Epstein-Barr virus-encoded LMP1 variant (2117-LMP1) in nasopharyngeal epithelial cells
dc.typeArticle
Author Affiliations
  1. The University of Hong Kong
  2. Prince of Wales Hospital Hong Kong