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Background  Hepatitis C virus (HCV) core protein and nonstructural protein 4B (NS4B) are potentially oncogenic. Aberrant activation of the Wnt/β-catenin signaling pathway is closely associated with hepatocarcinogenesis. We investigated the effects of HCV type 1b core protein and NS4B on Wnt/β-catenin signaling in various liver cells, and explored the molecular mechanism underlying HCV-related hepatocarcinogenesis.    Results  Compared with the empty vector control, HCV core protein and NS4B demonstrated the following characteristics in the Huh7 cells: significantly enhanced β-catenin/Tcf-dependent transcriptional activity ( F  = 40.87,  P  < 0.01); increased nuclear translocation of β-catenin ( F  = 165.26,  P  < 0.01); upregulated nuclear β-catenin, cytoplasmic β-catenin, Wnt1, c-myc, and cyclin D1 protein expression ( P  < 0.01); and promoted proliferation of Huh7 cells ( P  < 0.01 or  P  < 0.05). Neither protein enhanced β-catenin/Tcf-dependent transcriptional activity in the LO2 cells ( F  = 0.65,  P  > 0.05), but they did significantly enhance Wnt3a-induced β-catenin/Tcf-dependent transcriptional activity ( F  = 64.25,  P  < 0.01), and promoted the nuclear translocation of β-catenin ( F  = 66.54,  P  < 0.01) and the Wnt3a-induced proliferation of LO2 cells ( P  < 0.01 or  P  < 0.05). Moreover, activation of the Wnt/β-catenin signaling pathway was greater with the core protein than with NS4B ( P  < 0.01 or  P  < 0.05).    Conclusions  HCV core protein and NS4B directly activate the Wnt/β-catenin signaling pathway in Huh7 cells and LO2 cells induced by Wnt3a. These data suggest that HCV core protein and NS4B contribute to HCV-associated hepatocellular carcinogenesis.    Electronic supplementary material  The online version of this article (doi:10.1186/s12866-017-1032-4) contains supplementary material, which is available to authorized users.

Effects of hepatitis C virus core protein and nonstructural protein 4B on the Wnt/β-catenin pathway