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Hepatitis B virus X protein induced expression of the Nur77 gene.

Authors
Lee, MO; Kang, HJ; Cho, H; Shin, EC; Park, JH; Kim, SJ
Citation
Biochemical and biophysical research communications, 288(5):1162-1168, 2001
Journal Title
Biochemical and biophysical research communications
ISSN
0006-291X1090-2104
Abstract
Hepatitis B virus (HBV) X protein (HBx) plays an essential role in development of HBV-associated hepatocellular carcinoma (HCC). Recently, we reported that HBx induces Fas Ligand (FasL) expression, which may help HCC cells to evade host-immune surveillance. The aim of this study was to investigate the role of HBx in expression of Nur77, an orphan nuclear receptor implicated in the upregulation of FasL. When Chang X-34 expressing HBx under the control of a doxycycline-inducible promoter was examined, induction of Nur77 was observed following HBx expression. Blocking of Nur77 function by introduction of an antisense or a dominant negative mutant Nur77 significantly inhibited the induction of FasL, indicating that Nur77 plays critical roles in FasL expression. Further, a high-level expression of transcripts and DNA binding of Nur77 were observed in the HBV-integrated cell lines established from HCC patients that express HBx. These results suggested that Nur77 may contribute to leading the HBx-induced Fas/FasL signaling pathway which eliminates invading Fas-expressing lymphocytes.
MeSH terms
Carcinoma, Hepatocellular/geneticsCarcinoma, Hepatocellular/metabolism*Carcinoma, Hepatocellular/virologyDNA-Binding Proteins/biosynthesis*DNA-Binding Proteins/geneticsDNA-Binding Proteins/physiologyFas Ligand ProteinHepatitis B/geneticsHepatitis B/metabolism*Hepatitis B/virologyHepatitis B virus/geneticsHumansLiver Neoplasms/geneticsLiver Neoplasms/metabolism*Liver Neoplasms/virologyMembrane Glycoproteins/biosynthesisMembrane Glycoproteins/geneticsMutationNuclear Receptor Subfamily 4, Group A, Member 1Oligonucleotides, Antisense/pharmacologyPromoter Regions, GeneticRNA, Messenger/biosynthesisReceptors, Cytoplasmic and NuclearReceptors, SteroidTrans-Activators/biosynthesisTrans-Activators/geneticsTrans-Activators/metabolismTrans-Activators/pharmacology*Trans-Activators/physiologyTranscription Factors/biosynthesis*Transcription Factors/geneticsTranscription Factors/physiologyTranscriptional Activation*TransfectionTumor Cells, Cultured
DOI
10.1006/bbrc.2001.5910
PMID
11700033
Appears in Collections:
Journal Papers > School of Medicine / Graduate School of Medicine > Biochemistry & Molecular Biology
AJOU Authors
조, 혜성
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