Hepatitis C virus core protein promotes cell proliferation through the upregulation of cyclin E expression levels
- 1 April 2001
- journal article
- research article
- Published by Wiley in Liver International
- Vol. 21 (2), 137-142
- https://doi.org/10.1034/j.1600-0676.2001.021002137.x
Abstract
Aims/Background: The hepatitis C virus (HCV) core protein is known to play an important role in hepatocarcinogenesis. Recent studies have suggested that the increased proliferation rate of hepatocytes is a major risk factor for the development of hepatocellular carcinoma. In this study, we investigated whether the HCV core protein promotes the cell growth rate through the modulation of cyclin E expression levels. Methods/Results: HCV core stable transfectant Rat‐1 cell lines showed a markedly increased proliferation rate compared to mock cells. Cyclin E expression and its associated kinase activities were remarkably increased in HCV core stable transfectants. Cyclin E mRNA levels were also upregulated in these cell lines. Conclusions: Our data suggest that the HCV core protein promotes cell proliferation through upregulation of the cyclin E expression levels, implying this property of HCV core protein plays an important role in hepatocarcinogenesis.Keywords
This publication has 27 references indexed in Scilit:
- Natural history of hepatitis CHepatology, 1997
- Hepatitis C and hepatocellular carcinomaHepatology, 1997
- Transcriptional Repression of p53 Promoter by Hepatitis C Virus Core ProteinPublished by Elsevier BV ,1997
- Cancer Cell CyclesScience, 1996
- Inhibitors of mammalian G1 cyclin-dependent kinases.Genes & Development, 1995
- The retinoblastoma protein and cell cycle controlCell, 1995
- Genomic Typing of Hepatitis C Viruses from Korean Patients: Implications of Genome Variation in the E2/NS1 RegionBiochemical and Biophysical Research Communications, 1993
- Mammalian G1 cyclinsCell, 1993
- Cyclin-Dependent Regulation of G 1 in Mammalian FibroblastsScience, 1993
- Formation and Activation of a Cyclin E-cdk2 Complex During the G 1 Phase of the Human Cell CycleScience, 1992