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

TitleEpstein-Barr virus infection alters cellular signal cascades in human nasopharyngeal epithelial cells
Authors
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
Citation
Neoplasia, 2006, v. 8 n. 3, p. 173-180 How to Cite?
Abstract
Epstein-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.
Persistent Identifierhttp://hdl.handle.net/10722/48947
ISSN
2013 Impact Factor: 5.398
2013 SCImago Journal Rankings: 3.140
PubMed Central ID
ISI Accession Number ID

 

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
DC FieldValueLanguage
dc.contributor.authorLo, AKFen_HK
dc.contributor.authorLo, KWen_HK
dc.contributor.authorTsao, SWen_HK
dc.contributor.authorWong, HLen_HK
dc.contributor.authorHui, JWYen_HK
dc.contributor.authorTo, KFen_HK
dc.contributor.authorHayward, SDen_HK
dc.contributor.authorChui, YLen_HK
dc.contributor.authorLau, YLen_HK
dc.contributor.authorTakada, Ken_HK
dc.contributor.authorHuang, DPen_HK
dc.date.accessioned2008-06-12T06:30:26Z-
dc.date.available2008-06-12T06:30:26Z-
dc.date.issued2006en_HK
dc.identifier.citationNeoplasia, 2006, v. 8 n. 3, p. 173-180en_HK
dc.identifier.issn1522-8002en_HK
dc.identifier.urihttp://hdl.handle.net/10722/48947-
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.en_HK
dc.format.extent388 bytes-
dc.format.mimetypetext/html-
dc.languageengen_HK
dc.publisherNeoplasia Press. The Journal's web site is located at http://www.neoplasia.orgen_HK
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.subjectNasopharyngeal carcinomaen_HK
dc.subjectEpstein-Barr virusen_HK
dc.subjectNFκBen_HK
dc.subjectSTAT3en_HK
dc.subjectCell signalingen_HK
dc.titleEpstein-Barr virus infection alters cellular signal cascades in human nasopharyngeal epithelial cellsen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1522-8002&volume=8&issue=3&spage=173&epage=180&date=2006&atitle=Epstein-Barr+virus+infection+alters+cellular+signal+cascades+in+human+nasopharyngeal+epithelial+cellsen_HK
dc.identifier.emailTsao, SW: gswtsao@hkucc.hku.hken_HK
dc.identifier.emailWong, HL: giant20_00@yahoo.comen_HK
dc.identifier.emailLau, YL: lauylung@hkucc.hku.hken_HK
dc.description.naturepublished_or_final_versionen_HK
dc.identifier.doi10.1593/neo.05625en_HK
dc.identifier.pmid16611410en_HK
dc.identifier.pmcidPMC1578522en_HK
dc.identifier.scopuseid_2-s2.0-33646338489-
dc.identifier.hkuros116624-
dc.identifier.isiWOS:000239282800002-
dc.identifier.citeulike580506-

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