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
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
2011 Impact Factor: 3.641
2011 SCImago Journal Rankings: 0.516
ISI Accession Number IDWOS:000183114700010
ReferencesReferences in Scopus
DC Field
Value
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
2011 Impact Factor: 3.641
2011 SCImago Journal Rankings: 0.516
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
Author Affiliations
  1. The University of Hong Kong
  2. Prince of Wales Hospital Hong Kong