Antimigratory Effects of the Methanol Extract from Momordica charantia on Human Lung Adenocarcinoma CL1 Cells

Figure 6

Proposed mechanism for MCME-mediated inhibition against migration of CL1 cells. The effect of MCME is mediated by both Src/FAK and Wnt signaling pathways. MCME reduces the expression and activation of Src and FAK, leading to the decreased expression of Akt which regulates the phosphorylation of GSK-3β. MCME-induced inactivation of GSK-3β is also regulated by the increased Wnt-2 after treatment. Declined expressions of β-catenin and MMPs demonstrate that antimetastatic activity of MCME-treated CL1 cells is mainly mediated through Src/FAK/Akt, but not Wnt-2/GSK-3β, pathway to inhibit β-catenin from entering the nucleus. In conclusion, Src, FAK, PI3K/Akt, and β-catenin are involved in the critical pathway to inhibit the metastasis through the downregulation of MMPs on MCME-treated CL1 cells.