Fig. 9From: MICAL2 contributes to gastric cancer cell migration via Cdc42-dependent activation of E-cadherin/β-catenin signaling pathwaySchematic model for how MICAL2 regulates E-cadherin degradation and β-catenin-mediated cell migration. In brief, MICAL2 was identified as a novel key molecule implicated in gastric cancer cell migration. MICAL2 increased E-cadherin ubiquitination and degradation in a Cdc42-dependent manner, thereby leading to enhanced β-catenin signaling via the disruption of the E-cadherin/β-catenin complex and, consequently, the promotion of gastric cell migrationBack to article page