Abstract:
:Hepatitis C virus (HCV) infection often leads to the development of hepatocellular carcinoma (HCC), but its molecular mechanism has not been clearly elucidated. Previously, transgenic mice constitutively expressing HCV core protein have been shown to develop HCC, suggesting a pivotal role of the core protein in hepatocarcinogenesis. Here, we analyzed the expression of cytokines associated with a variety of cellular processes, including cell proliferation, in the mouse model for HCV-associated HCC to define the molecular events prior to oncogenesis. The expression of tumor necrosis factor-alpha and interleukin-1beta was increased at both protein and mRNA levels. In addition, the activities of c-Jun N-terminal kinase and activator protein-1 (AP-1), downstream effectors, were enhanced, while IkappaB kinase or nuclear factor-kappaB activities were not enhanced. Thus, the altered in vivo expression of cytokines with AP-1 activation in consequence to the core protein expression may contribute to hepatocarcinogenesis in persistent HCV infection.
journal_name
Virologyjournal_title
Virologyauthors
Tsutsumi T,Suzuki T,Moriya K,Yotsuyanagi H,Shintani Y,Fujie H,Matsuura Y,Kimura S,Koike K,Miyamura Tdoi
10.1006/viro.2002.1702subject
Has Abstractpub_date
2002-12-20 00:00:00pages
415-24issue
2eissn
0042-6822issn
1096-0341pii
S0042682202917022journal_volume
304pub_type
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