Fig. 2

Molecular mechanisms and functions of the Wnt/β-catenin signalling pathway in HFSCs. a In the absence of a Wnt signal for the binding of Wnt inhibitors (e.g., sFRP1, Dkk3, or Wif), a multiprotein complex is formed with APC, Axin, and GSK3, which can target and phosphorylate β-catenin, leading to excessive cytoplasmic β-catenin degradation. b Once Wnt binds to Frizzled and lipoprotein receptor-related protein (Lrp5/6 receptors), the activated receptor complex induces recruitment of certain key components, such as Dvl, which results in the destruction complex disassembling, to prevent β-catenin degradation. Accumulated and stabilized β-catenin is translocated to the nucleus, where it can bind transcription factors (e.g., LEF/TCF family) to promote the expression of target genes, such as Axin2, LEF1 and Lgr5. c Wnt signalling shows a close association with HFSCs in quiescence, activation, and differentiation and even in Wnt-induced tumorigenesis. The T-shaped lines indicate inhibitory interactions involved in this pathway, and the solid arrows indicate activating interactions