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Article: COOH-terminal truncated HBV X protein plays key role in hepatocarcinogenesis

TitleCOOH-terminal truncated HBV X protein plays key role in hepatocarcinogenesis
Authors
Issue Date2008
PublisherAmerican Association for Cancer Research
Citation
Clinical Cancer Research, 2008, v. 14 n. 16, p. 5061-5068 How to Cite?
AbstractPurpose: X protein (HBx), a product of hepatitis B virus, has been closely associated with the development of hepatocellular carcinoma (HCC). Based on observations that the COOH-terminal truncated HBx was frequently detected in HCC, the aim of this study is to evaluate the function of COOH-terminal truncated HBx in hepatocarcinogenesis. Experimental Design: Expression pattern of HBx was analyzed by immunohistochemistry on tissue microarray containing 194 pairs of HCCs and their matched nontumor liver tissues. MIHA and HepG2 cells transfected with full-length (X2) and COOH-terminal truncated HBx (X1) were tested for their ability to grow in soft agar and form tumors in vivo. Proliferation and apoptosis were assessed using 2,3-bis[2-methoxy-4-nitro-5- sulfophenyl]-2H-tetrazolium-5-carboxanilide inner salt and terminal deoxyribonucleotidyl transferase-mediated dUTP nick-end labeling assays, respectively. To gain additional insight, the expression profile of HepG2-X2 and HepG2-X1 were compared using cDNA microarray. Results: COOH-terminal truncated HBx was frequently detected in HCCs (79.3%, n = 111), and our in vitro and in vivo studies showed that the truncated rather than the full-length HBx could effectively transform immortalized liver cell line MIHA. Interestingly, expression profiling revealed differential expression of key genes implicated in the control of cell cycle and apoptosis. Conclusions: These findings strongly suggest that the COOH-terminal truncated HBx plays a critical role in the HCC carcinogenesis via the activation of cell proliferation. © 2008 American Association for Cancer Research.
Persistent Identifierhttp://hdl.handle.net/10722/58606
ISSN
2015 Impact Factor: 8.738
2015 SCImago Journal Rankings: 5.314
ISI Accession Number ID
Funding AgencyGrant Number
Control of Infectious Diseases RFCID02040162
Sun Yat-Sen University85000-3171311
Major State Basic Research Program of China2006CB910104
Foundation of Guangzhou Science and Technology Bureau2005Z1-E0131
Funding Information:

Research Fund for the Control of Infectious Diseases RFCID (02040162), Sun Yat-Sen University "Hundred Talents Program" (85000-3171311), the Major State Basic Research Program of China (2006CB910104), and the Foundation of Guangzhou Science and Technology Bureau (<INF>2005Z1-EO131</INF>).

References
Grants

 

DC FieldValueLanguage
dc.contributor.authorNingFang, Men_HK
dc.contributor.authorLau, SHen_HK
dc.contributor.authorHu, Len_HK
dc.contributor.authorXie, Den_HK
dc.contributor.authorWu, Jen_HK
dc.contributor.authorYang, Jen_HK
dc.contributor.authorWang, Yen_HK
dc.contributor.authorWu, MCen_HK
dc.contributor.authorFung, Jen_HK
dc.contributor.authorBai, Xen_HK
dc.contributor.authorTzang, CHen_HK
dc.contributor.authorFu, Len_HK
dc.contributor.authorYang, Men_HK
dc.contributor.authorSu, YAen_HK
dc.contributor.authorGuan, XYen_HK
dc.date.accessioned2010-05-31T03:33:23Z-
dc.date.available2010-05-31T03:33:23Z-
dc.date.issued2008en_HK
dc.identifier.citationClinical Cancer Research, 2008, v. 14 n. 16, p. 5061-5068en_HK
dc.identifier.issn1078-0432en_HK
dc.identifier.urihttp://hdl.handle.net/10722/58606-
dc.description.abstractPurpose: X protein (HBx), a product of hepatitis B virus, has been closely associated with the development of hepatocellular carcinoma (HCC). Based on observations that the COOH-terminal truncated HBx was frequently detected in HCC, the aim of this study is to evaluate the function of COOH-terminal truncated HBx in hepatocarcinogenesis. Experimental Design: Expression pattern of HBx was analyzed by immunohistochemistry on tissue microarray containing 194 pairs of HCCs and their matched nontumor liver tissues. MIHA and HepG2 cells transfected with full-length (X2) and COOH-terminal truncated HBx (X1) were tested for their ability to grow in soft agar and form tumors in vivo. Proliferation and apoptosis were assessed using 2,3-bis[2-methoxy-4-nitro-5- sulfophenyl]-2H-tetrazolium-5-carboxanilide inner salt and terminal deoxyribonucleotidyl transferase-mediated dUTP nick-end labeling assays, respectively. To gain additional insight, the expression profile of HepG2-X2 and HepG2-X1 were compared using cDNA microarray. Results: COOH-terminal truncated HBx was frequently detected in HCCs (79.3%, n = 111), and our in vitro and in vivo studies showed that the truncated rather than the full-length HBx could effectively transform immortalized liver cell line MIHA. Interestingly, expression profiling revealed differential expression of key genes implicated in the control of cell cycle and apoptosis. Conclusions: These findings strongly suggest that the COOH-terminal truncated HBx plays a critical role in the HCC carcinogenesis via the activation of cell proliferation. © 2008 American Association for Cancer Research.en_HK
dc.languageengen_HK
dc.publisherAmerican Association for Cancer Researchen_HK
dc.relation.ispartofClinical Cancer Researchen_HK
dc.titleCOOH-terminal truncated HBV X protein plays key role in hepatocarcinogenesisen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1078-0432&volume=14&spage=5061&epage=8&date=2008&atitle=COOH-terminal+truncated+HBV+X+protein+plays+key+role+in+hepatocarcinogenesisen_HK
dc.identifier.emailGuan, XY:xyguan@hkucc.hku.hken_HK
dc.identifier.authorityGuan, XY=rp00454en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1158/1078-0432.CCR-07-5082en_HK
dc.identifier.pmid18698024-
dc.identifier.scopuseid_2-s2.0-52649139395en_HK
dc.identifier.hkuros150603en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-52649139395&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume14en_HK
dc.identifier.issue16en_HK
dc.identifier.spage5061en_HK
dc.identifier.epage5068en_HK
dc.identifier.isiWOS:000258523800009-
dc.publisher.placeUnited Statesen_HK
dc.relation.projectOncogeneic role of hepatitis B Virus (HBV) X gene in the development of hepatocellular carcinoma-
dc.identifier.scopusauthoridNingFang, M=36123694300en_HK
dc.identifier.scopusauthoridLau, SH=7401596190en_HK
dc.identifier.scopusauthoridHu, L=34770075600en_HK
dc.identifier.scopusauthoridXie, D=35070710200en_HK
dc.identifier.scopusauthoridWu, J=35228235500en_HK
dc.identifier.scopusauthoridYang, J=33968246200en_HK
dc.identifier.scopusauthoridWang, Y=7601486269en_HK
dc.identifier.scopusauthoridWu, MC=7405593399en_HK
dc.identifier.scopusauthoridFung, J=23469161200en_HK
dc.identifier.scopusauthoridBai, X=16308787500en_HK
dc.identifier.scopusauthoridTzang, CH=6508203245en_HK
dc.identifier.scopusauthoridFu, L=36631373600en_HK
dc.identifier.scopusauthoridYang, M=7404925734en_HK
dc.identifier.scopusauthoridSu, YA=36814427400en_HK
dc.identifier.scopusauthoridGuan, XY=7201463221en_HK

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