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Article: Latent membrane protein-1 of Epstein-Barr virus inhibits cell growth and induces sensitivity to cisplatin in nasopharyngeal carcinoma cells

TitleLatent membrane protein-1 of Epstein-Barr virus inhibits cell growth and induces sensitivity to cisplatin in nasopharyngeal carcinoma cells
Authors
KeywordsBax
Bcl-2
Carcinoma
Cisplatin
LMP1
Nasopharyngeal
Issue Date2002
PublisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/32763
Citation
Journal Of Medical Virology, 2002, v. 66 n. 1, p. 63-69 How to Cite?
AbstractNasopharyngeal carcinoma is closely associated with Epstein-Barr virus (EBV) and the EBV encoded latent membrane protein-1 expression (LMP1) is commonly found in the tumour cells. LMP1 has been shown to be involved in modulation of cell growth in B cells but the biological properties of LMP1 expression in nasopharyngeal carcinoma cells are less defined. In this study, a full length LMP1 gene was introduced into an EBV negative nasopharyngeal carcinoma cell line, CNE2, and five LMPl-expressing clones were isolated. Expression of LMP1 did not confer cell growth advantage in CNE2 cells; instead, it induced growth inhibition both in vitro and in vivo. In addition, the LMP1 transfected cells were more susceptible to cisplatin-induced cell death and showed 1.4-4.0-fold increased sensitivity to cisplatin compared to the vector infected control clones. The effect of LMP1 on the balance of Bcl-2 and Bax ratio may play a role in inducing susceptibility to cisplatin-induced cell death. These results demonstrated that LMP1 did not confer growth advantage in CNE2 cells, suggesting that expression of LMP1 may not be crucial in sustaining cell growth in established cell lines. Alternatively, LMP1 alone may not be sufficient to facilitate nasopharyngeal carcinoma cell growth and additional oncogenic factors may be needed along with LMP1 in modulating the malignant property of nasopharyngeal carcinoma. © 2002 Wiley-Liss, Inc.
Persistent Identifierhttp://hdl.handle.net/10722/67362
ISSN
2023 Impact Factor: 6.8
2023 SCImago Journal Rankings: 1.560
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLiu, Yen_HK
dc.contributor.authorWang, Xen_HK
dc.contributor.authorLo, AKFen_HK
dc.contributor.authorWong, YCen_HK
dc.contributor.authorCheung, ALMen_HK
dc.contributor.authorTsao, SWen_HK
dc.date.accessioned2010-09-06T05:54:27Z-
dc.date.available2010-09-06T05:54:27Z-
dc.date.issued2002en_HK
dc.identifier.citationJournal Of Medical Virology, 2002, v. 66 n. 1, p. 63-69en_HK
dc.identifier.issn0146-6615en_HK
dc.identifier.urihttp://hdl.handle.net/10722/67362-
dc.description.abstractNasopharyngeal carcinoma is closely associated with Epstein-Barr virus (EBV) and the EBV encoded latent membrane protein-1 expression (LMP1) is commonly found in the tumour cells. LMP1 has been shown to be involved in modulation of cell growth in B cells but the biological properties of LMP1 expression in nasopharyngeal carcinoma cells are less defined. In this study, a full length LMP1 gene was introduced into an EBV negative nasopharyngeal carcinoma cell line, CNE2, and five LMPl-expressing clones were isolated. Expression of LMP1 did not confer cell growth advantage in CNE2 cells; instead, it induced growth inhibition both in vitro and in vivo. In addition, the LMP1 transfected cells were more susceptible to cisplatin-induced cell death and showed 1.4-4.0-fold increased sensitivity to cisplatin compared to the vector infected control clones. The effect of LMP1 on the balance of Bcl-2 and Bax ratio may play a role in inducing susceptibility to cisplatin-induced cell death. These results demonstrated that LMP1 did not confer growth advantage in CNE2 cells, suggesting that expression of LMP1 may not be crucial in sustaining cell growth in established cell lines. Alternatively, LMP1 alone may not be sufficient to facilitate nasopharyngeal carcinoma cell growth and additional oncogenic factors may be needed along with LMP1 in modulating the malignant property of nasopharyngeal carcinoma. © 2002 Wiley-Liss, Inc.en_HK
dc.languageengen_HK
dc.publisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/32763en_HK
dc.relation.ispartofJournal of Medical Virologyen_HK
dc.rightsJournal of Medical Virology. Copyright © John Wiley & Sons, Inc.en_HK
dc.subjectBax-
dc.subjectBcl-2-
dc.subjectCarcinoma-
dc.subjectCisplatin-
dc.subjectLMP1-
dc.subjectNasopharyngeal-
dc.subject.meshAntineoplastic Agents - pharmacologyen_HK
dc.subject.meshCell Divisionen_HK
dc.subject.meshCisplatin - pharmacologyen_HK
dc.subject.meshHerpesvirus 4, Human - metabolismen_HK
dc.subject.meshHumansen_HK
dc.subject.meshIntracellular Signaling Peptides and Proteinsen_HK
dc.subject.meshNasopharyngeal Neoplasms - genetics - metabolism - pathologyen_HK
dc.subject.meshNuclear Proteinsen_HK
dc.subject.meshProteins - genetics - metabolismen_HK
dc.subject.meshProto-Oncogene Proteins - genetics - metabolismen_HK
dc.subject.meshProto-Oncogene Proteins c-bcl-2 - genetics - metabolismen_HK
dc.subject.meshTransfectionen_HK
dc.subject.meshTumor Cells, Cultureden_HK
dc.subject.meshViral Matrix Proteins - genetics - metabolism - physiologyen_HK
dc.subject.meshbcl-2-Associated X Proteinen_HK
dc.titleLatent membrane protein-1 of Epstein-Barr virus inhibits cell growth and induces sensitivity to cisplatin in nasopharyngeal carcinoma cellsen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0146-6615&volume=66&spage=63&epage=69&date=2002&atitle=Latent+membrane+protein-1+of+epstein-barr+virus+inhibits+cell+growth+and+induces+sensitivity+to+cisplatin+in+nasopharyngeal+carcinoma+cellsen_HK
dc.identifier.emailWong, YC:ycwong@hkucc.hku.hken_HK
dc.identifier.emailCheung, ALM:lmcheung@hkucc.hku.hken_HK
dc.identifier.emailTsao, SW:gswtsao@hkucc.hku.hken_HK
dc.identifier.authorityWong, YC=rp00316en_HK
dc.identifier.authorityCheung, ALM=rp00332en_HK
dc.identifier.authorityTsao, SW=rp00399en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1002/jmv.2112en_HK
dc.identifier.pmid11748660-
dc.identifier.scopuseid_2-s2.0-0036186372en_HK
dc.identifier.hkuros74658en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0036186372&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume66en_HK
dc.identifier.issue1en_HK
dc.identifier.spage63en_HK
dc.identifier.epage69en_HK
dc.identifier.isiWOS:000172560100010-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridLiu, Y=26643293600en_HK
dc.identifier.scopusauthoridWang, X=7501854829en_HK
dc.identifier.scopusauthoridLo, AKF=7102780657en_HK
dc.identifier.scopusauthoridWong, YC=7403041798en_HK
dc.identifier.scopusauthoridCheung, ALM=7401806497en_HK
dc.identifier.scopusauthoridTsao, SW=7102813116en_HK
dc.identifier.issnl0146-6615-

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