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.
Publication types
-
Research Support, Non-U.S. Gov't
MeSH terms
-
Anti-Bacterial Agents / pharmacology
-
Anti-Infective Agents / pharmacology
-
Blotting, Western
-
Cell Division / physiology*
-
Cell Survival / physiology*
-
Chloramphenicol O-Acetyltransferase / metabolism
-
Colony-Forming Units Assay
-
Gene Expression Regulation
-
Hepatitis B Antigens / metabolism
-
Hepatitis B Antigens / pharmacology*
-
Humans
-
I-kappa B Proteins / pharmacology
-
Liver / physiology
-
NF-kappa B / metabolism*
-
Promoter Regions, Genetic
-
Proto-Oncogene Proteins c-rel
-
RNA, Messenger / metabolism
-
Sulfasalazine / pharmacology
-
Tetracyclines
-
Thymidine / metabolism
-
Trans-Activators / metabolism
-
Trans-Activators / pharmacology*
-
Transcription Factor AP-1
-
Transcription, Genetic
-
Transcriptional Activation
-
Viral Regulatory and Accessory Proteins
Substances
-
Anti-Bacterial Agents
-
Anti-Infective Agents
-
Hepatitis B Antigens
-
I-kappa B Proteins
-
NF-kappa B
-
Proto-Oncogene Proteins c-rel
-
RNA, Messenger
-
Tetracyclines
-
Trans-Activators
-
Transcription Factor AP-1
-
Viral Regulatory and Accessory Proteins
-
hepatitis B virus X protein
-
Sulfasalazine
-
Chloramphenicol O-Acetyltransferase
-
Thymidine