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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

TitleAlterations of biologic properties and gene expression in nasopharyngeal epithelial cells by the Epstein-Barr virus-encoded latent membrane protein 1
Authors
Issue Date2003
PublisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/labinvest/
Citation
Laboratory Investigation, 2003, v. 83 n. 5, p. 697-709 How to Cite?
Abstract
Undifferentiated 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.
Persistent Identifierhttp://hdl.handle.net/10722/149617
ISSN
2013 Impact Factor: 3.828
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLo, AKFen_US
dc.contributor.authorLiu, Yen_US
dc.contributor.authorWang, XHen_US
dc.contributor.authorHuang, DPen_US
dc.contributor.authorYuen, PWen_US
dc.contributor.authorWong, YCen_US
dc.contributor.authorTsao, GSWen_US
dc.date.accessioned2012-06-26T05:56:05Z-
dc.date.available2012-06-26T05:56:05Z-
dc.date.issued2003en_US
dc.identifier.citationLaboratory Investigation, 2003, v. 83 n. 5, p. 697-709en_US
dc.identifier.issn0023-6837en_US
dc.identifier.urihttp://hdl.handle.net/10722/149617-
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.en_US
dc.languageengen_US
dc.publisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/labinvest/en_US
dc.relation.ispartofLaboratory Investigationen_US
dc.subject.meshBlotting, Westernen_US
dc.subject.meshCell Differentiationen_US
dc.subject.meshCell Divisionen_US
dc.subject.meshCell Lineen_US
dc.subject.meshCell Movementen_US
dc.subject.meshCell Survivalen_US
dc.subject.meshEpithelial Cells - Metabolism - Pathologyen_US
dc.subject.meshGene Expression Profilingen_US
dc.subject.meshHumansen_US
dc.subject.meshMitogen-Activated Protein Kinases - Metabolismen_US
dc.subject.meshNasopharyngeal Neoplasms - Etiologyen_US
dc.subject.meshNasopharynx - Metabolism - Pathologyen_US
dc.subject.meshNeoplasm Invasivenessen_US
dc.subject.meshOligonucleotide Array Sequence Analysisen_US
dc.subject.meshViral Matrix Proteins - Physiologyen_US
dc.subject.meshRas Proteins - Metabolismen_US
dc.titleAlterations of biologic properties and gene expression in nasopharyngeal epithelial cells by the Epstein-Barr virus-encoded latent membrane protein 1en_US
dc.typeArticleen_US
dc.identifier.emailWong, YC:ycwong@hkucc.hku.hken_US
dc.identifier.emailTsao, GSW:gswtsao@hkucc.hku.hken_US
dc.identifier.authorityWong, YC=rp00316en_US
dc.identifier.authorityTsao, GSW=rp00399en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.pmid12746479en_US
dc.identifier.scopuseid_2-s2.0-0038814052en_US
dc.identifier.hkuros76480-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0038814052&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume83en_US
dc.identifier.issue5en_US
dc.identifier.spage697en_US
dc.identifier.epage709en_US
dc.identifier.isiWOS:000183114700010-
dc.publisher.placeUnited Kingdomen_US
dc.identifier.scopusauthoridLo, AKF=7102780657en_US
dc.identifier.scopusauthoridLiu, Y=26643293600en_US
dc.identifier.scopusauthoridWang, XH=7501854829en_US
dc.identifier.scopusauthoridHuang, DP=7403891486en_US
dc.identifier.scopusauthoridYuen, PW=7103124007en_US
dc.identifier.scopusauthoridWong, YC=7403041798en_US
dc.identifier.scopusauthoridTsao, GSW=7102813116en_US

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