Fig. 7

Hypothesied pathway showing the inhibitory mechanism of cyclin G2 on Wnt/β-catenin signaling through Dpr1. a Wnt ligands bind to Fzd and LRP co-receptor complexes, which in turn activates Dvl2. Dvl2 inhibits the activity of GSK-3β triggering β-catenin phosphorylation and preventing its degradation. Stabilized β-catenin activates gene expression of the Wnt/β-catenin signaling pathway and upregulates tumorigenesis. The inhibitory effect of Dpr1 on the Wnt/β-catenin signaling is blocked when phosphorylated by CKI. b Cyclin G2 interacts with Dpr1 and impacts its phosphorylation level, enhancing proteasome-dependent degradation of Dvl2. As a result, increasing the ability of GSK-3β to phosphorylate β-catenin and accelerate its degradation. This leads to suppression of Wnt/β-catenin signaling and inhibition of tumorigenesis of gastric cancer