Fig. 7

ALX4 inhibited the progression of breast cancer via promoting phosphorylation degradation of β-catenin in a GSK3β dependent manner. a The expression of ALX4 and β-catenin was analyzed by WB 48 h after transfection with control vector or β-catenin over expression vector in MDA-MB-231-ALX4 cells. b MTS assays were used to examine the effect of β-catenin re-expression on cell proliferation in MDA-MB-231-ALX4 cells. c Transwell assays were used to examine the effect of β-catenin re-expression on cell metastasis of MDA-MB-231-ALX4 cell. d The expression of ALX4 and GSK3β was analyzed by WB 48 h after transfection with control vector or GSK3β siRNA vector in MDA-MB-231-ALX4 cells. e MTS assays were used to examine the effect of GSK3β knock down on cell proliferation in MDA-MB-231-ALX4 cells. f Transwell assays were used to examine the effect of GSK3β knock down on cell metastasis in MDA-MB-231-ALX4 cell. g Schematic diagram of the mechanisms of ALX4 mediated suppression of breast cancer cell proliferation and metastasis based on our study. ALX4 reduces the protein level of β-catenin by promoting its phosphorylation degradation via up regulation of GSK3β, which subsequently inhibits the activation of Wnt/β-catenin signaling