Figure 1.

Wnt signalling in the adult quiescent liver and in CTNNB1-mutated HCCs. (a) The liver-cell plate and its portocentral organization; (b) the periportal hepatocyte is deprived of Wnt signalling, due to its high amount of Apc, allowing the destruction complex to be efficient to degrade β-catenin. The pericentral hepatocyte has a Wnt-dependent β-catenin signalling, while in HCCs it is constitutively activated due to mutations in phosphorylation residues in CTNNB1; (c) the output of the transcriptional β-catenin is metabolic in the pericentral hepatocyte, while it is both metabolic and mitogenic in HCCs.