Article: Epstein-Barr virus infection alters cellular signal cascades in human nasopharyngeal epithelial cells

File Download Links for fulltext
(May Require Subscription)
Supplementary
  • Basic View
  • Metadata View
  • XML View
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
2011 Impact Factor: 5.946
2011 SCImago Journal Rankings: 0.667
DOIhttp://dx.doi.org/10.1593/neo.05625
ISI Accession Number IDWOS:000239282800002
PubMed Central IDPMC1578522
DC Field
Value
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
2011 Impact Factor: 5.946
2011 SCImago Journal Rankings: 0.667
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
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