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NF-kappaB activation by hepatitis B virus X (HBx) protein shifts the cellular fate toward survival.

Authors
Yun, C; Um, HR; Jin, YH; Wang, JH; Lee, MO; Park, S; Lee, JH; Cho, H
Citation
Cancer letters, 184(1):97-104, 2002
Journal Title
Cancer letters
ISSN
0304-38351872-7980
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.
MeSH terms
Anti-Bacterial Agents/pharmacologyAnti-Infective Agents/pharmacologyBlotting, WesternCell Division/*physiologyCell Survival/*physiologyChloramphenicol O-Acetyltransferase/metabolismColony-Forming Units AssayGene Expression RegulationHepatitis B Antigens/metabolism/*pharmacologyHumansI-kappa B Proteins/pharmacologyLiver/physiologyNF-kappa B/*metabolismPromoter Regions, GeneticProto-Oncogene Proteins c-relRNA, Messenger/metabolismSulfasalazine/pharmacologyTetracyclinesThymidine/metabolismTrans-Activators/metabolism/*pharmacologyTranscription Factor AP-1Transcription, GeneticTranscriptional Activation
PMID
12104053
Appears in Collections:
Journal Papers > School of Medicine / Graduate School of Medicine > Biochemistry & Molecular Biology
Journal Papers > School of Medicine / Graduate School of Medicine > Microbiology
AJOU Authors
윤, 차원박, 선이, 재호조, 혜성
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