Activation of the CKI-CDK-Rb-E2F Pathway in Full Genome Hepatitis C Virus-expressing Cells
Copyright policy )Activation of the CKI-CDK-Rb-E2F Pathway in Full Genome Hepatitis C Virus-expressing Cells
Hepatitis C virus (HCV) causes persistent infection in hepatocytes, and this infection is, in turn, strongly associated with the development of hepatocellular carcinoma. To clarify the mechanisms underlying these effects, we established a Cre/loxP conditional expression system for the precisely self-trimmed HCV genome in human liver cells. Passage of hepatocytes expressing replicable full-length HCV (HCR6-Rz) RNA caused up-regulation of anchorage-independent growth after 44 days. In contrast, hepatocytes expressing HCV structural, nonstructural, or all viral proteins showed no significant changes after passage for 44 days. Only cells expressing HCR6-Rz passaged for 44 days displayed acceleration of CDK activity, hyperphosphorylation of Rb, and E2F activation. These results demonstrate that full genome HCV expression up-regulates the CDK-Rb-E2F pathway much more effectively than HCV proteins during passage.
- Showa University Japan
- University of Tokyo Japan
- Tokyo Metropolitan Institute of Medical Science Japan
- Institute of Medical Science Japan
- Max Planck Society Germany
Cyclin-Dependent Kinase Inhibitor p21, Gene Expression Regulation, Viral, DNA, Complementary, Blotting, Western, Cell Cycle, Cell Cycle Proteins, Cell Separation, Genome, Viral, Hepacivirus, Flow Cytometry, Cyclin-Dependent Kinases, Cell Line, E2F Transcription Factors, DNA-Binding Proteins, Genes, Reporter, Cyclins, Hepatocytes, Cloning, Molecular, Casein Kinases, Cell Division
Cyclin-Dependent Kinase Inhibitor p21, Gene Expression Regulation, Viral, DNA, Complementary, Blotting, Western, Cell Cycle, Cell Cycle Proteins, Cell Separation, Genome, Viral, Hepacivirus, Flow Cytometry, Cyclin-Dependent Kinases, Cell Line, E2F Transcription Factors, DNA-Binding Proteins, Genes, Reporter, Cyclins, Hepatocytes, Cloning, Molecular, Casein Kinases, Cell Division
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