title: NF-kappaB activation by hepatitis B virus X (HBx) protein shifts the cellular fate toward survival.
abstract: In this paper, we examined the cellular effect of hepatitits B virus X (HBx) in ChangX-34 cells, inducible HBx-expressing cells. High expression of HBx protein in ChangX-34 cells resulted in approximately three-fold increase in DNA synthesis and did not show apoptotic changes. Expression of HBx in these cells was accompanied by the NF-kappaB-mediated transcription. Interestingly, inhibition of NF-kappaB activity either by treatment with sulfasalazine, a specific inhibitor of NF-kappaB, or by expressing IkappaBalpha super-repressor significantly increased cell death in ChangX-34 cells but had no influence on parental Chang cells. Thus, the activation of NF-kappaB in HBx-expressing cells may play a critical role in shifting the balance toward cell survival.
authors.affiliation: Department of Biochemistry, Ajou University School of Medicine, Suwon 442-749, South Korea.
authors.forename: Chawon
authors.initials: C
authors.lastname: Yun
authors.forename: Hae Ryun
authors.initials: HR
authors.lastname: Um
authors.forename: Young Hee
authors.initials: YH
authors.lastname: Jin
authors.forename: Jin-Hee
authors.initials: JH
authors.lastname: Wang
authors.forename: Mi-Ock
authors.initials: MO
authors.lastname: Lee
authors.forename: Sun
authors.initials: S
authors.lastname: Park
authors.forename: Jae-Ho
authors.initials: JH
authors.lastname: Lee
authors.forename: Hyeseong
authors.initials: H
authors.lastname: Cho
mesh_terms: D000900:Anti-Bacterial Agents / Q000494:pharmacology; D000890:Anti-Infective Agents / Q000494:pharmacology; D015153:Blotting, Western; D002455:Cell Division / Q000502:physiology*; D002470:Cell Survival / Q000502:physiology*; D015500:Chloramphenicol O-Acetyltransferase / Q000378:metabolism; D003114:Colony-Forming Units Assay; D005786:Gene Expression Regulation; D006511:Hepatitis B Antigens / Q000378:metabolism / Q000494:pharmacology*; D006801:Humans; D020672:I-kappa B Proteins / Q000494:pharmacology; D008099:Liver / Q000502:physiology; D016328:NF-kappa B / Q000378:metabolism*; D011401:Promoter Regions, Genetic; D020569:Proto-Oncogene Proteins c-rel; D012333:RNA, Messenger / Q000378:metabolism; D012460:Sulfasalazine / Q000494:pharmacology; D013754:Tetracyclines; D013936:Thymidine / Q000378:metabolism; D015534:Trans-Activators / Q000378:metabolism / Q000494:pharmacology*; D018808:Transcription Factor AP-1; D014158:Transcription, Genetic; D015533:Transcriptional Activation; D054334:Viral Regulatory and Accessory Proteins
chemical_list: D000900:Anti-Bacterial Agents; D000890:Anti-Infective Agents; D006511:Hepatitis B Antigens; D020672:I-kappa B Proteins; D016328:NF-kappa B; D020569:Proto-Oncogene Proteins c-rel; D012333:RNA, Messenger; D013754:Tetracyclines; D015534:Trans-Activators; D018808:Transcription Factor AP-1; D054334:Viral Regulatory and Accessory Proteins; C057628:hepatitis B virus X protein; D012460:Sulfasalazine; D015500:Chloramphenicol O-Acetyltransferase; D013936:Thymidine