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. 2022 Apr 10;14(8):1912. doi: 10.3390/cancers14081912

Figure 1.

Figure 1

Wnt/β-Catenin-dependent signaling. (a) In the OFF state, or absence of Wnt ligand, cytoplasmic β-catenin undergoes phosphorylation by the destruction complex (composed of Axin, APC, CK-1, and GSK-3). This leads to degradation of β-catenin in the proteosome after being ubiquitinated by β-TrCP. In the nucleus, transcription of target genes is repressed through the TLE-1 complex with TCF/LEF. (b) In the ON state, porcine acylase (PORCN) o-acylates Wnt ligands and facilitates their secretion and interaction with receptors. Binding of Wnt to the Frizzled receptor causes phosphorylation of the LRP co-receptor by CK1 and GSK3. Dvl protein is recruited to the plasma membrane and blocks the β-catenin destruction complex. This causes β-catenin to accumulate in the cytoplasm and then translocate to the nucleus, where it forms a complex with TCF/LEF to transcribe its target genes (i.e., cyclin D1, c-Myc, vascular endothelial growth factor (VEGF), interleukin-8 (IL-8), etc.).