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Article: Epstein-Barr virus infection alters cellular signal cascades in human nasopharyngeal epithelial cells
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TitleEpstein-Barr virus infection alters cellular signal cascades in human nasopharyngeal epithelial cells
 
AuthorsLo, AKF2 3
Lo, KW
Tsao, SW1
Wong, HL
Hui, JWY2
To, KF
Hayward, SD3
Chui, YL
Lau, YL1
Takada, K4
Huang, DP2
 
KeywordsNasopharyngeal carcinoma
Epstein-Barr virus
NFκB
STAT3
Cell signaling
 
Issue Date2006
 
PublisherNeoplasia Press. The Journal's web site is located at http://www.neoplasia.org
 
CitationNeoplasia, 2006, v. 8 n. 3, p. 173-180 [How to Cite?]
DOI: http://dx.doi.org/10.1593/neo.05625
 
AbstractEpstein-Barr virus (EBV) latent infection is a critical event in nasopharyngeal carcinoma (NPC) tumorigenesis. EBV-encoded genes have been shown to be involved in immune evasion and in the regulation of various cellular signaling cascades. To elucidate the roles of EBV in NPC development, stable infection of EBV in nasopharyngeal epithelial cell lines was established. Similar to primary tumors of NPC, these infected cells exhibited a type II EBV latency expression pattern. In this study, multiple cellular signaling pathways in EBV-infected cells were investigated. We first demonstrated that in vitro EBV infection resulted in the activation of STAT3 and NFkappaB signal cascades in nasopharyngeal epithelial cells. Increased expression of their downstream targets (c-Myc, Bcl-xL, IL-6, LIF, SOCS-1, SOCS-3, VEGF, and COX-2) was also observed. Moreover, EBV latent infection induced the suppression of p38-MAPK activities, but did not activate PKR cascade. Our findings suggest that EBV latent infection is able to manipulate multiple cellular signal cascades to protect infected cells from immunologic attack and to facilitate cancer development.
 
ISSN1522-8002
2012 Impact Factor: 5.47
2012 SCImago Journal Rankings: 2.615
 
DOIhttp://dx.doi.org/10.1593/neo.05625
 
PubMed Central IDPMC1578522
 
ISI Accession Number IDWOS:000239282800002
 
DC FieldValue
dc.contributor.authorLo, AKF
 
dc.contributor.authorLo, KW
 
dc.contributor.authorTsao, SW
 
dc.contributor.authorWong, HL
 
dc.contributor.authorHui, JWY
 
dc.contributor.authorTo, KF
 
dc.contributor.authorHayward, SD
 
dc.contributor.authorChui, YL
 
dc.contributor.authorLau, YL
 
dc.contributor.authorTakada, K
 
dc.contributor.authorHuang, DP
 
dc.date.accessioned2008-06-12T06:30:26Z
 
dc.date.available2008-06-12T06:30:26Z
 
dc.date.issued2006
 
dc.description.abstractEpstein-Barr virus (EBV) latent infection is a critical event in nasopharyngeal carcinoma (NPC) tumorigenesis. EBV-encoded genes have been shown to be involved in immune evasion and in the regulation of various cellular signaling cascades. To elucidate the roles of EBV in NPC development, stable infection of EBV in nasopharyngeal epithelial cell lines was established. Similar to primary tumors of NPC, these infected cells exhibited a type II EBV latency expression pattern. In this study, multiple cellular signaling pathways in EBV-infected cells were investigated. We first demonstrated that in vitro EBV infection resulted in the activation of STAT3 and NFkappaB signal cascades in nasopharyngeal epithelial cells. Increased expression of their downstream targets (c-Myc, Bcl-xL, IL-6, LIF, SOCS-1, SOCS-3, VEGF, and COX-2) was also observed. Moreover, EBV latent infection induced the suppression of p38-MAPK activities, but did not activate PKR cascade. Our findings suggest that EBV latent infection is able to manipulate multiple cellular signal cascades to protect infected cells from immunologic attack and to facilitate cancer development.
 
dc.description.naturepublished_or_final_version
 
dc.format.extent388 bytes
 
dc.format.mimetypetext/html
 
dc.identifier.citationNeoplasia, 2006, v. 8 n. 3, p. 173-180 [How to Cite?]
DOI: http://dx.doi.org/10.1593/neo.05625
 
dc.identifier.citeulike580506
 
dc.identifier.doihttp://dx.doi.org/10.1593/neo.05625
 
dc.identifier.hkuros116624
 
dc.identifier.isiWOS:000239282800002
 
dc.identifier.issn1522-8002
2012 Impact Factor: 5.47
2012 SCImago Journal Rankings: 2.615
 
dc.identifier.openurl
 
dc.identifier.pmcidPMC1578522
 
dc.identifier.pmid16611410
 
dc.identifier.scopuseid_2-s2.0-33646338489
 
dc.identifier.urihttp://hdl.handle.net/10722/48947
 
dc.languageeng
 
dc.publisherNeoplasia Press. The Journal's web site is located at http://www.neoplasia.org
 
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License
 
dc.subjectNasopharyngeal carcinoma
 
dc.subjectEpstein-Barr virus
 
dc.subjectNFκB
 
dc.subjectSTAT3
 
dc.subjectCell signaling
 
dc.titleEpstein-Barr virus infection alters cellular signal cascades in human nasopharyngeal epithelial cells
 
dc.typeArticle
 
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<contributor.author>Hayward, SD</contributor.author>
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Author Affiliations
  1. The University of Hong Kong
  2. Prince of Wales Hospital Hong Kong
  3. The Johns Hopkins School of Medicine
  4. Hokkaido University