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Article: Alterations of biologic properties and gene expression in nasopharyngeal epithelial cells by the Epstein-Barr virus-encoded latent membrane protein 1
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TitleAlterations of biologic properties and gene expression in nasopharyngeal epithelial cells by the Epstein-Barr virus-encoded latent membrane protein 1
 
AuthorsLo, AKF1
Liu, Y1
Wang, XH1
Huang, DP2
Yuen, PW1
Wong, YC1
Tsao, GSW1 1
 
Issue Date2003
 
PublisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/labinvest/
 
CitationLaboratory Investigation, 2003, v. 83 n. 5, p. 697-709 [How to Cite?]
 
AbstractUndifferentiated nasopharyngeal carcinoma (NPC) is closely associated with EBV infection, and the EBV-encoded latent membrane protein 1 (LMP1) is frequently detected in NPC. However, little is known about the pathologic roles of LMP1 in this disease. Recently, we reported the morphologic transformation and increased expression of the LAMC2 and ITGα6 genes in LMP1-expressing NPC cell lines. In this study, we further examine the effects of LMP1 in an immortalized nasopharyngeal epithelial cell line called NP69. This cell line was established from primary nonmalignant nasopharyngeal epithelial cells and may represent a model of premalignant nasopharyngeal epithelial cells. LMP1 induced many phenotypic changes in NP69 cells. These include morphologic transformation, increased cell proliferation, anchorage-independent growth, resistance to serum free-induced cell death, and enhanced cell migration and invasion. In addition, expression array analysis identified 28 genes that demonstrated a more than 2-fold difference in expression of NP69 cells expressing LMP1 when compared with a vector control. Two of the up-regulated genes (VEGF and vimentin) identified have been previously reported as LMP1 targets. The majority of the identified genes are associated with cell growth, differentiation, cell shape, and invasion. The present findings support the proposed roles of LMP1 in promoting cell transformation, migration, and invasion in premalignant nasopharyngeal epithelial cells. The present study also indicates the activation of the Ras/MAPK pathway in LMP1-expressing cells, which may be involved in mediating some of the transforming effects of LMP1 observed in nasopharyngeal epithelial cells.
 
ISSN0023-6837
2012 Impact Factor: 3.961
2012 SCImago Journal Rankings: 1.448
 
ISI Accession Number IDWOS:000183114700010
 
ReferencesReferences in Scopus
 
DC FieldValue
dc.contributor.authorLo, AKF
 
dc.contributor.authorLiu, Y
 
dc.contributor.authorWang, XH
 
dc.contributor.authorHuang, DP
 
dc.contributor.authorYuen, PW
 
dc.contributor.authorWong, YC
 
dc.contributor.authorTsao, GSW
 
dc.date.accessioned2012-06-26T05:56:05Z
 
dc.date.available2012-06-26T05:56:05Z
 
dc.date.issued2003
 
dc.description.abstractUndifferentiated nasopharyngeal carcinoma (NPC) is closely associated with EBV infection, and the EBV-encoded latent membrane protein 1 (LMP1) is frequently detected in NPC. However, little is known about the pathologic roles of LMP1 in this disease. Recently, we reported the morphologic transformation and increased expression of the LAMC2 and ITGα6 genes in LMP1-expressing NPC cell lines. In this study, we further examine the effects of LMP1 in an immortalized nasopharyngeal epithelial cell line called NP69. This cell line was established from primary nonmalignant nasopharyngeal epithelial cells and may represent a model of premalignant nasopharyngeal epithelial cells. LMP1 induced many phenotypic changes in NP69 cells. These include morphologic transformation, increased cell proliferation, anchorage-independent growth, resistance to serum free-induced cell death, and enhanced cell migration and invasion. In addition, expression array analysis identified 28 genes that demonstrated a more than 2-fold difference in expression of NP69 cells expressing LMP1 when compared with a vector control. Two of the up-regulated genes (VEGF and vimentin) identified have been previously reported as LMP1 targets. The majority of the identified genes are associated with cell growth, differentiation, cell shape, and invasion. The present findings support the proposed roles of LMP1 in promoting cell transformation, migration, and invasion in premalignant nasopharyngeal epithelial cells. The present study also indicates the activation of the Ras/MAPK pathway in LMP1-expressing cells, which may be involved in mediating some of the transforming effects of LMP1 observed in nasopharyngeal epithelial cells.
 
dc.description.natureLink_to_subscribed_fulltext
 
dc.identifier.citationLaboratory Investigation, 2003, v. 83 n. 5, p. 697-709 [How to Cite?]
 
dc.identifier.epage709
 
dc.identifier.hkuros76480
 
dc.identifier.isiWOS:000183114700010
 
dc.identifier.issn0023-6837
2012 Impact Factor: 3.961
2012 SCImago Journal Rankings: 1.448
 
dc.identifier.issue5
 
dc.identifier.pmid12746479
 
dc.identifier.scopuseid_2-s2.0-0038814052
 
dc.identifier.spage697
 
dc.identifier.urihttp://hdl.handle.net/10722/149617
 
dc.identifier.volume83
 
dc.languageeng
 
dc.publisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/labinvest/
 
dc.publisher.placeUnited Kingdom
 
dc.relation.ispartofLaboratory Investigation
 
dc.relation.referencesReferences in Scopus
 
dc.subject.meshBlotting, Western
 
dc.subject.meshCell Differentiation
 
dc.subject.meshCell Division
 
dc.subject.meshCell Line
 
dc.subject.meshCell Movement
 
dc.subject.meshCell Survival
 
dc.subject.meshEpithelial Cells - Metabolism - Pathology
 
dc.subject.meshGene Expression Profiling
 
dc.subject.meshHumans
 
dc.subject.meshMitogen-Activated Protein Kinases - Metabolism
 
dc.subject.meshNasopharyngeal Neoplasms - Etiology
 
dc.subject.meshNasopharynx - Metabolism - Pathology
 
dc.subject.meshNeoplasm Invasiveness
 
dc.subject.meshOligonucleotide Array Sequence Analysis
 
dc.subject.meshViral Matrix Proteins - Physiology
 
dc.subject.meshRas Proteins - Metabolism
 
dc.titleAlterations of biologic properties and gene expression in nasopharyngeal epithelial cells by the Epstein-Barr virus-encoded latent membrane protein 1
 
dc.typeArticle
 
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Author Affiliations
  1. The University of Hong Kong
  2. Prince of Wales Hospital Hong Kong