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Action and function of Wnt/?-catenin signaling in the progression from chronic
hepatitis C to hepatocellular carcinoma
#MMPMID28035485
Wang W
; Pan Q
; Fuhler GM
; Smits R
; Peppelenbosch MP
J Gastroenterol
2017[Apr]; 52
(4
): 419-431
PMID28035485
show ga
Hepatitis C virus (HCV) infection is one of the leading causes of hepatocellular
carcinoma (HCC) worldwide but the mechanistic basis as to how chronic HCV
infection furthers the HCC process remains only poorly understood. Accumulating
evidence indicates that HCV core and nonstructural proteins provoke activation of
the Wnt/?-catenin signaling pathway, and the evidence supporting a role of
Wnt/?-catenin signaling in the onset and progression of HCC is compelling.
Convincing molecular explanations as to how expression of viral effectors
translates into increased activity of the Wnt/?-catenin signaling machinery are
still largely lacking, hampering the design of rational strategies aimed at
preventing HCC. Furthermore, how such increased signaling is especially
associated with HCC oncogenesis in the context of HCV infection remains obscure
as well. Here we review the body of contemporary biomedical knowledge on the role
of the Wnt/?-catenin pathway in the progression from chronic hepatitis C to
cirrhosis and HCC and explore potential hypotheses as to the mechanisms involved.