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Conference Paper: HBV X gene is required for maintaining the tumorigenicity of hepatocellular carcinoma cells

TitleHBV X gene is required for maintaining the tumorigenicity of hepatocellular carcinoma cells
Authors
Issue Date2004
PublisherAmerican Association for Cancer Research
Citation
AACR 95th Annual Meeting, Orlando FL, 27–31 March 2004. In Cancer Research, 2004, v. 64 n. 7S, p. 362 Abstract no. 1573 How to Cite?
AbstractHepatitis B virus (HBV) infection is a major cause of human hepatocellular carcinoma (HCC) in Southeast Asia and Hong Kong. Among the four proteins that originate from the HBV genome, HBV X (HBx) is the most potentially oncogenic factor. Despite the extensive studies on the roles of HBx in the development of HCC, the precise mechanism of HBx in tumor formation is still unclear and remains controversial. However, the expression of HBx in the majority of HCC cases strongly suggests that it may play a critical role in maintaining the tumorigenicity of HCC. In this study, we used stably transfected vector-derived short hairpin RNAs (shRNAs) to knock down the expression of HBx in PLC/PRF/5 HCC cell line which constitutively produces HBx. Preliminary data showed that this tool could successfully reduce HBx mRNA levels by 70-95% in PLC/PRF/5 cells. Inhibition of HBx expression in PLC/PRF/5 cells significantly reduced the cell growth rate in low serum medium and the ability of anchorage-independent growth in soft agar. Besides, suppressing the expression of HBx caused decreased expression levels of c-myc and Bcl-XL. Furthermore, by immunofluorenscence microscopy, we found that there was less amount of NF-κB localized in the nuclei of the PLC/PRF/5 cells that exhibited reduced levels of HBx expression due to RNAi. Hence, we propose that HBx might maintain tumorigenicity of HCC cells by inducing NF-κB nuclear translocalization that is associated with the transcriptional activation of the expression of c-myc, Bcl-XL and perhaps of other oncogenes.
Persistent Identifierhttp://hdl.handle.net/10722/104463
ISSN
2015 Impact Factor: 8.556
2015 SCImago Journal Rankings: 5.372

 

DC FieldValueLanguage
dc.contributor.authorChan, DWen_HK
dc.contributor.authorNg, IOLen_HK
dc.date.accessioned2010-09-25T21:54:06Z-
dc.date.available2010-09-25T21:54:06Z-
dc.date.issued2004en_HK
dc.identifier.citationAACR 95th Annual Meeting, Orlando FL, 27–31 March 2004. In Cancer Research, 2004, v. 64 n. 7S, p. 362 Abstract no. 1573-
dc.identifier.issn0008-5472-
dc.identifier.urihttp://hdl.handle.net/10722/104463-
dc.description.abstractHepatitis B virus (HBV) infection is a major cause of human hepatocellular carcinoma (HCC) in Southeast Asia and Hong Kong. Among the four proteins that originate from the HBV genome, HBV X (HBx) is the most potentially oncogenic factor. Despite the extensive studies on the roles of HBx in the development of HCC, the precise mechanism of HBx in tumor formation is still unclear and remains controversial. However, the expression of HBx in the majority of HCC cases strongly suggests that it may play a critical role in maintaining the tumorigenicity of HCC. In this study, we used stably transfected vector-derived short hairpin RNAs (shRNAs) to knock down the expression of HBx in PLC/PRF/5 HCC cell line which constitutively produces HBx. Preliminary data showed that this tool could successfully reduce HBx mRNA levels by 70-95% in PLC/PRF/5 cells. Inhibition of HBx expression in PLC/PRF/5 cells significantly reduced the cell growth rate in low serum medium and the ability of anchorage-independent growth in soft agar. Besides, suppressing the expression of HBx caused decreased expression levels of c-myc and Bcl-XL. Furthermore, by immunofluorenscence microscopy, we found that there was less amount of NF-κB localized in the nuclei of the PLC/PRF/5 cells that exhibited reduced levels of HBx expression due to RNAi. Hence, we propose that HBx might maintain tumorigenicity of HCC cells by inducing NF-κB nuclear translocalization that is associated with the transcriptional activation of the expression of c-myc, Bcl-XL and perhaps of other oncogenes.-
dc.languageengen_HK
dc.publisherAmerican Association for Cancer Research-
dc.relation.ispartofCancer Researchen_HK
dc.titleHBV X gene is required for maintaining the tumorigenicity of hepatocellular carcinoma cellsen_HK
dc.typeConference_Paperen_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.identifier.hkuros86117en_HK

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