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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
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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
2013 Impact Factor: 5.007
 
DOIhttp://dx.doi.org/10.1002/ijc.20051
 
ISI Accession Number IDWOS:000220779200015
 
ReferencesReferences in Scopus
 
DC FieldValue
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
2013 Impact Factor: 5.007
 
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
 
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<description.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-&#954;B 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. &#169; 2004 Wiley-Liss, Inc.</description.abstract>
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<subject.mesh>Up-Regulation</subject.mesh>
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Author Affiliations
  1. The University of Hong Kong
  2. Prince of Wales Hospital Hong Kong