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Article: Knock-down of hepatitis B virus X protein reduces the tumorigenicity of hepatocellular carcinoma cells

TitleKnock-down of hepatitis B virus X protein reduces the tumorigenicity of hepatocellular carcinoma cells
Authors
KeywordsCell proliferation
Cell transformation
Hepatitis B virus X protein
Hepatocellular carcinoma
RNA interference
Tumour growth
Issue Date2006
PublisherJohn Wiley & Sons. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/1130
Citation
Journal Of Pathology, 2006, v. 208 n. 3, p. 372-380 How to Cite?
AbstractHepatitis B virus (HBV) infection is a major cause of hepatocellular carcinoma (HCC) in Southeast Asia and Hong Kong. Among the four proteins that are encoded by the HBV genome, HBV X (HBx) is the most potentially oncogenic factor. It is known that HBx plays an important role in hepatocarcinogenesis, but the exact functions and molecular mechanisms of HBx in HCC are not well understood. In this study, we constructed expression vectors for small hairpin RNAs (shRNA) against HBx and investigated their regulatory effects in PLC/PRF/5 HCC cells, which constitutively produce HBx. Our data show that this tool of RNA interference (RNAi) could successfully reduce the HBx mRNA and protein levels by 50-95%. RNAi targeting HBx in PLC/PRF/5 cells demonstrated significant reduction in cell proliferation, cell growth, anchorage-independent growth in soft agar, and tumour development in nude mice. In addition, depletion of HBx expression increased cell sensitivity to TNFα-mediated and serum-free-induced apoptosis, and reduced the expression levels of C-myc and Bcl-XL. These findings suggest that HBx plays an important role in tumorigenicity and anti-apoptosic mechanisms in HCC. Copyright © 2005 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
Persistent Identifierhttp://hdl.handle.net/10722/88653
ISSN
2015 Impact Factor: 7.381
2015 SCImago Journal Rankings: 4.176
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorChan, DWen_HK
dc.contributor.authorNg, IOLen_HK
dc.date.accessioned2010-09-06T09:46:11Z-
dc.date.available2010-09-06T09:46:11Z-
dc.date.issued2006en_HK
dc.identifier.citationJournal Of Pathology, 2006, v. 208 n. 3, p. 372-380en_HK
dc.identifier.issn0022-3417en_HK
dc.identifier.urihttp://hdl.handle.net/10722/88653-
dc.description.abstractHepatitis B virus (HBV) infection is a major cause of hepatocellular carcinoma (HCC) in Southeast Asia and Hong Kong. Among the four proteins that are encoded by the HBV genome, HBV X (HBx) is the most potentially oncogenic factor. It is known that HBx plays an important role in hepatocarcinogenesis, but the exact functions and molecular mechanisms of HBx in HCC are not well understood. In this study, we constructed expression vectors for small hairpin RNAs (shRNA) against HBx and investigated their regulatory effects in PLC/PRF/5 HCC cells, which constitutively produce HBx. Our data show that this tool of RNA interference (RNAi) could successfully reduce the HBx mRNA and protein levels by 50-95%. RNAi targeting HBx in PLC/PRF/5 cells demonstrated significant reduction in cell proliferation, cell growth, anchorage-independent growth in soft agar, and tumour development in nude mice. In addition, depletion of HBx expression increased cell sensitivity to TNFα-mediated and serum-free-induced apoptosis, and reduced the expression levels of C-myc and Bcl-XL. These findings suggest that HBx plays an important role in tumorigenicity and anti-apoptosic mechanisms in HCC. Copyright © 2005 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.en_HK
dc.languageengen_HK
dc.publisherJohn Wiley & Sons. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/1130en_HK
dc.relation.ispartofJournal of Pathologyen_HK
dc.rightsJournal of Pathology. Copyright © John Wiley & Sons Ltd.en_HK
dc.subjectCell proliferationen_HK
dc.subjectCell transformationen_HK
dc.subjectHepatitis B virus X proteinen_HK
dc.subjectHepatocellular carcinomaen_HK
dc.subjectRNA interferenceen_HK
dc.subjectTumour growthen_HK
dc.subject.meshAnimalsen_HK
dc.subject.meshApoptosis - geneticsen_HK
dc.subject.meshBlotting, Western - methodsen_HK
dc.subject.meshCarcinogenicity Testsen_HK
dc.subject.meshCarcinoma, Hepatocellular - genetics - pathologyen_HK
dc.subject.meshCell Line, Tumoren_HK
dc.subject.meshCell Proliferationen_HK
dc.subject.meshGene Expressionen_HK
dc.subject.meshGenetic Vectors - genetics - pharmacologyen_HK
dc.subject.meshHumansen_HK
dc.subject.meshLiver Neoplasms - genetics - pathologyen_HK
dc.subject.meshLiver Neoplasms, Experimentalen_HK
dc.subject.meshMiceen_HK
dc.subject.meshMice, Nudeen_HK
dc.subject.meshRNA - analysisen_HK
dc.subject.meshRNA Interferenceen_HK
dc.subject.meshRNA, Small Interfering - geneticsen_HK
dc.subject.meshTrans-Activators - geneticsen_HK
dc.subject.meshTransduction, Genetic - methodsen_HK
dc.titleKnock-down of hepatitis B virus X protein reduces the tumorigenicity of hepatocellular carcinoma cellsen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0022-3417&volume=208&issue=3&spage=372&epage=80&date=2006&atitle=Knock-down+of+hepatitis+B+virus+X+protein+reduces+the+tumorigenicity+of+hepatocellular+carcinoma+cellsen_HK
dc.identifier.emailChan, DW:dwchan@hkucc.hku.hken_HK
dc.identifier.emailNg, IOL:iolng@hkucc.hku.hken_HK
dc.identifier.authorityChan, DW=rp00543en_HK
dc.identifier.authorityNg, IOL=rp00335en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1002/path.1901en_HK
dc.identifier.pmid16353167-
dc.identifier.scopuseid_2-s2.0-32244445762en_HK
dc.identifier.hkuros114072en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-32244445762&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume208en_HK
dc.identifier.issue3en_HK
dc.identifier.spage372en_HK
dc.identifier.epage380en_HK
dc.identifier.isiWOS:000235374500007-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridChan, DW=26533900600en_HK
dc.identifier.scopusauthoridNg, IOL=7102753722en_HK

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