Activation of the CKI-CDK-Rb-E2F Pathway in Full Genome Hepatitis C 
Virus-expressing Cells

Tsukiyama-Kohara, Kyoko; Toné, Shigenobu; Maruyama, Isao; Inoue, Kazuaki; Katsume, Asao; Nuriya, Hideko; Ohmori, Hiroshi; Ohkawa, Jun; Taira, Kazunari; Hoshikawa, Yutaka; Shibasaki, Futoshi; Reth, Michael; Minatogawa, Yohsuke; Kohara, Michinori

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Activation of the CKI-CDK-Rb-E2F Pathway in Full Genome Hepatitis C Virus-expressing Cells

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Reth, Michael
Research Group and Chair of Molecular Immunology of the University of Freiburg, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

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Citation

Tsukiyama-Kohara, K., Toné, S., Maruyama, I., Inoue, K., Katsume, A., Nuriya, H., et al. (2004). Activation of the CKI-CDK-Rb-E2F Pathway in Full Genome Hepatitis C Virus-expressing Cells. The Journal of Biological Chemistry, 279, 14531-14541.

Cite as: https://hdl.handle.net/11858/00-001M-0000-002B-9437-7

Abstract

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.