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Interferon alpha inhibits the nuclear factor kappa B activation triggered by X gene product of hepatitis B virus in human hepatoma cells
Author(s) -
Ohata Kazuyuki,
Ichikawa Tatsuki,
Nakao Kazuhiko,
Shigeno Masaya,
Nishimura Daisuke,
Ishikawa Hiroki,
Hamasaki Keisuke,
Eguchi Katsumi
Publication year - 2003
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(03)01034-2
Subject(s) - hbx , hepatitis b virus , interferon , gene , nfkb1 , biology , gene product , transcription factor , alpha interferon , virus , mutant , microbiology and biotechnology , transcription (linguistics) , iκb kinase , alpha (finance) , cancer research , virology , gene expression , medicine , genetics , linguistics , philosophy , construct validity , nursing , patient satisfaction
X gene product of hepatitis B virus (HBV) (HBx) regulates many transcription factors including nuclear factor kappa B (NF‐κB) and plays a key role in hepatocarcinogenesis. In this study, we demonstrated that the expression of full HBV genome and HBx gene similarly stimulated the transcriptional activity of NF‐κB in HuH‐7 human hepatoma cells, and that interferon (IFN)‐α as well as dominant negative mutant of IκB kinase‐α effectively inhibited the HBx‐mediated NF‐κB activation, but IFN‐γ did not. These results suggest that IFN‐α may have a function to block the NF‐κB activating pathway triggered by HBx in HBV hepatocytes.