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Article: Epstein-Barr virus latent membrane protein 1 (LMP1) upregulates Id1 expression in nasopharyngeal epithelial cells

TitleEpstein-Barr virus latent membrane protein 1 (LMP1) upregulates Id1 expression in nasopharyngeal epithelial cells
Authors
KeywordsEpstein-Barr virus
Id1
LMP1
Nasopharyngeal carcinoma
Nuclear factor κB
Issue Date2004
PublisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/onc
Citation
Oncogene, 2004, v. 23 n. 25, p. 4488-4494 How to Cite?
AbstractNasopharyngeal carcinoma is closely associated with Epstein-Barr virus (EBV) infection. The EBV-encoded LMP1 has cell transformation property. It suppresses cellular senescence and enhances cell survival in various cell types. Many of the downstream events of LMP1 expression are mediated through its ability to activate NF-κB. In this study, we report a novel function of LMP1 to induce Id1 expression in nasopharyngeal epithelial cells (NP69) and human embryonal kidney cells (HEK293). The Id1 is a basic helix-loop-helix (bHLH) protein and a negative transcriptional regulator of p16INK4a. Expression of Id1 facilitates cellular immortalization and stimulates cell proliferation. With the combination of both specific chemical inhibitors and genetic inhibitors of cell signaling, we showed that induction of Id1 by LMP1 was dependent on its NF-κB activation domain at the carboxy-terminal region, CTAR1 and CTAR2. Induction of Id1 by LMP1 may facilitate clonal expansion of premalignant nasopharyngeal epithelial cells infected with EBV and may promote their malignant transformation.
Persistent Identifierhttp://hdl.handle.net/10722/67704
ISSN
2015 Impact Factor: 7.932
2015 SCImago Journal Rankings: 4.047
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLi, HMen_HK
dc.contributor.authorZhuang, Zhen_HK
dc.contributor.authorWang, Qen_HK
dc.contributor.authorPang, JCSen_HK
dc.contributor.authorWang, XHen_HK
dc.contributor.authorWong, HLen_HK
dc.contributor.authorFeng, HCen_HK
dc.contributor.authorJin, DYen_HK
dc.contributor.authorLing, MTen_HK
dc.contributor.authorWong, YCen_HK
dc.contributor.authorEliopoulos, AGen_HK
dc.contributor.authorYoung, LSen_HK
dc.contributor.authorHuang, DPen_HK
dc.contributor.authorTsao, SWen_HK
dc.date.accessioned2010-09-06T05:57:30Z-
dc.date.available2010-09-06T05:57:30Z-
dc.date.issued2004en_HK
dc.identifier.citationOncogene, 2004, v. 23 n. 25, p. 4488-4494en_HK
dc.identifier.issn0950-9232en_HK
dc.identifier.urihttp://hdl.handle.net/10722/67704-
dc.description.abstractNasopharyngeal carcinoma is closely associated with Epstein-Barr virus (EBV) infection. The EBV-encoded LMP1 has cell transformation property. It suppresses cellular senescence and enhances cell survival in various cell types. Many of the downstream events of LMP1 expression are mediated through its ability to activate NF-κB. In this study, we report a novel function of LMP1 to induce Id1 expression in nasopharyngeal epithelial cells (NP69) and human embryonal kidney cells (HEK293). The Id1 is a basic helix-loop-helix (bHLH) protein and a negative transcriptional regulator of p16INK4a. Expression of Id1 facilitates cellular immortalization and stimulates cell proliferation. With the combination of both specific chemical inhibitors and genetic inhibitors of cell signaling, we showed that induction of Id1 by LMP1 was dependent on its NF-κB activation domain at the carboxy-terminal region, CTAR1 and CTAR2. Induction of Id1 by LMP1 may facilitate clonal expansion of premalignant nasopharyngeal epithelial cells infected with EBV and may promote their malignant transformation.en_HK
dc.languageengen_HK
dc.publisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/oncen_HK
dc.relation.ispartofOncogeneen_HK
dc.subjectEpstein-Barr virusen_HK
dc.subjectId1en_HK
dc.subjectLMP1en_HK
dc.subjectNasopharyngeal carcinomaen_HK
dc.subjectNuclear factor κBen_HK
dc.subject.meshCarcinoma - epidemiology - etiology - virologyen_HK
dc.subject.meshClone Cells - pathologyen_HK
dc.subject.meshCyclin-Dependent Kinase Inhibitor p16 - biosynthesisen_HK
dc.subject.meshEpithelial Cells - metabolism - virologyen_HK
dc.subject.meshEpstein-Barr Virus Infections - geneticsen_HK
dc.subject.meshGene Expression Regulation, Viralen_HK
dc.subject.meshGenes, p16en_HK
dc.subject.meshHerpesvirus 4, Human - physiologyen_HK
dc.subject.meshHong Kong - epidemiologyen_HK
dc.subject.meshHumansen_HK
dc.subject.meshInhibitor of Differentiation Protein 1en_HK
dc.subject.meshNF-kappa B - physiologyen_HK
dc.subject.meshNasopharyngeal Neoplasms - epidemiology - etiology - virologyen_HK
dc.subject.meshNasopharynx - cytologyen_HK
dc.subject.meshProtein Structure, Tertiaryen_HK
dc.subject.meshRepressor Proteinsen_HK
dc.subject.meshSequence Deletionen_HK
dc.subject.meshSignal Transductionen_HK
dc.subject.meshTranscription Factors - biosynthesis - genetics - physiologyen_HK
dc.subject.meshTranscription, Geneticen_HK
dc.subject.meshViral Matrix Proteins - chemistry - physiologyen_HK
dc.titleEpstein-Barr virus latent membrane protein 1 (LMP1) upregulates Id1 expression in nasopharyngeal epithelial cellsen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0950-9232&volume=23&spage=4488&epage=4494&date=2004&atitle=Epstein-Barr+virus+latent+membrane+protein+1+(LMP1)+upregulates+Id1+expression+in+nasopharyngeal+epithelial+cellsen_HK
dc.identifier.emailJin, DY:dyjin@hkucc.hku.hken_HK
dc.identifier.emailLing, MT:patling@hkucc.hku.hken_HK
dc.identifier.emailWong, YC:ycwong@hkucc.hku.hken_HK
dc.identifier.emailTsao, SW:gswtsao@hkucc.hku.hken_HK
dc.identifier.authorityJin, DY=rp00452en_HK
dc.identifier.authorityLing, MT=rp00449en_HK
dc.identifier.authorityWong, YC=rp00316en_HK
dc.identifier.authorityTsao, SW=rp00399en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1038/sj.onc.1207580en_HK
dc.identifier.pmid15064751en_HK
dc.identifier.scopuseid_2-s2.0-3042532226en_HK
dc.identifier.hkuros87586en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-3042532226&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume23en_HK
dc.identifier.issue25en_HK
dc.identifier.spage4488en_HK
dc.identifier.epage4494en_HK
dc.identifier.isiWOS:000221661300014-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridLi, HM=8312261000en_HK
dc.identifier.scopusauthoridZhuang, Zh=36880759000en_HK
dc.identifier.scopusauthoridWang, Q=7406910452en_HK
dc.identifier.scopusauthoridPang, JCS=7201733981en_HK
dc.identifier.scopusauthoridWang, XH=7501854829en_HK
dc.identifier.scopusauthoridWong, HL=7402862563en_HK
dc.identifier.scopusauthoridFeng, HC=7401736336en_HK
dc.identifier.scopusauthoridJin, DY=7201973614en_HK
dc.identifier.scopusauthoridLing, MT=7102229780en_HK
dc.identifier.scopusauthoridWong, YC=7403041798en_HK
dc.identifier.scopusauthoridEliopoulos, AG=7003973196en_HK
dc.identifier.scopusauthoridYoung, LS=7403664751en_HK
dc.identifier.scopusauthoridHuang, DP=7403891486en_HK
dc.identifier.scopusauthoridTsao, SW=7102813116en_HK

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