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- PMID: 16353167
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Article: Knock-down of hepatitis B virus X protein reduces the tumorigenicity of hepatocellular carcinoma cells
Title | Knock-down of hepatitis B virus X protein reduces the tumorigenicity of hepatocellular carcinoma cells |
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Authors | |
Keywords | Cell proliferation Cell transformation Hepatitis B virus X protein Hepatocellular carcinoma RNA interference Tumour growth |
Issue Date | 2006 |
Publisher | John 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? |
Abstract | Hepatitis 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 Identifier | http://hdl.handle.net/10722/88653 |
ISSN | 2023 Impact Factor: 5.6 2023 SCImago Journal Rankings: 2.426 |
ISI Accession Number ID | |
References |
DC Field | Value | Language |
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dc.contributor.author | Chan, DW | en_HK |
dc.contributor.author | Ng, IOL | en_HK |
dc.date.accessioned | 2010-09-06T09:46:11Z | - |
dc.date.available | 2010-09-06T09:46:11Z | - |
dc.date.issued | 2006 | en_HK |
dc.identifier.citation | Journal Of Pathology, 2006, v. 208 n. 3, p. 372-380 | en_HK |
dc.identifier.issn | 0022-3417 | en_HK |
dc.identifier.uri | http://hdl.handle.net/10722/88653 | - |
dc.description.abstract | Hepatitis 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.language | eng | en_HK |
dc.publisher | John Wiley & Sons. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/1130 | en_HK |
dc.relation.ispartof | Journal of Pathology | en_HK |
dc.rights | Journal of Pathology. Copyright © John Wiley & Sons Ltd. | en_HK |
dc.subject | Cell proliferation | en_HK |
dc.subject | Cell transformation | en_HK |
dc.subject | Hepatitis B virus X protein | en_HK |
dc.subject | Hepatocellular carcinoma | en_HK |
dc.subject | RNA interference | en_HK |
dc.subject | Tumour growth | en_HK |
dc.subject.mesh | Animals | en_HK |
dc.subject.mesh | Apoptosis - genetics | en_HK |
dc.subject.mesh | Blotting, Western - methods | en_HK |
dc.subject.mesh | Carcinogenicity Tests | en_HK |
dc.subject.mesh | Carcinoma, Hepatocellular - genetics - pathology | en_HK |
dc.subject.mesh | Cell Line, Tumor | en_HK |
dc.subject.mesh | Cell Proliferation | en_HK |
dc.subject.mesh | Gene Expression | en_HK |
dc.subject.mesh | Genetic Vectors - genetics - pharmacology | en_HK |
dc.subject.mesh | Humans | en_HK |
dc.subject.mesh | Liver Neoplasms - genetics - pathology | en_HK |
dc.subject.mesh | Liver Neoplasms, Experimental | en_HK |
dc.subject.mesh | Mice | en_HK |
dc.subject.mesh | Mice, Nude | en_HK |
dc.subject.mesh | RNA - analysis | en_HK |
dc.subject.mesh | RNA Interference | en_HK |
dc.subject.mesh | RNA, Small Interfering - genetics | en_HK |
dc.subject.mesh | Trans-Activators - genetics | en_HK |
dc.subject.mesh | Transduction, Genetic - methods | en_HK |
dc.title | Knock-down of hepatitis B virus X protein reduces the tumorigenicity of hepatocellular carcinoma cells | en_HK |
dc.type | Article | en_HK |
dc.identifier.openurl | http://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+cells | en_HK |
dc.identifier.email | Chan, DW:dwchan@hkucc.hku.hk | en_HK |
dc.identifier.email | Ng, IOL:iolng@hkucc.hku.hk | en_HK |
dc.identifier.authority | Chan, DW=rp00543 | en_HK |
dc.identifier.authority | Ng, IOL=rp00335 | en_HK |
dc.description.nature | link_to_subscribed_fulltext | - |
dc.identifier.doi | 10.1002/path.1901 | en_HK |
dc.identifier.pmid | 16353167 | - |
dc.identifier.scopus | eid_2-s2.0-32244445762 | en_HK |
dc.identifier.hkuros | 114072 | en_HK |
dc.relation.references | http://www.scopus.com/mlt/select.url?eid=2-s2.0-32244445762&selection=ref&src=s&origin=recordpage | en_HK |
dc.identifier.volume | 208 | en_HK |
dc.identifier.issue | 3 | en_HK |
dc.identifier.spage | 372 | en_HK |
dc.identifier.epage | 380 | en_HK |
dc.identifier.isi | WOS:000235374500007 | - |
dc.publisher.place | United Kingdom | en_HK |
dc.identifier.scopusauthorid | Chan, DW=26533900600 | en_HK |
dc.identifier.scopusauthorid | Ng, IOL=7102753722 | en_HK |
dc.identifier.issnl | 0022-3417 | - |