Figure 5.

The kinase activity of GSk3β regulates the strength of Ecad/Ecad bonds but only in the presence of β-catenin. (A) Upon shRNAi depletion of GSk3β, HCT116 cells expressing WT β-catenin (GSK3β-KD)β^WT/−) exhibit significantly weaker Ecad/Ecad bonds, whereas HCT116 cells expressing mutant β-catenin (GSk3β-KD)β^−/Δ45) do not show this weakening. Inhibition of GSk3β (using LiCl, β^WT/−/LiCl and β^−/ΔS45/LiCl) also weakened individual intercellular Ecad/Ecad bonds. ^∗∗∗ Designates p < 0.001, unpaired Student’s t-test. (B and C) In SW480 cells with endogenous APC mutation, genetic depletion of GSK3β (B) induces no change in the Ecad/Ecad bond strength (C), whereas depletion of endogenous WT β-catenin causes significant weakening of Ecad/Ecad bonds. All bars designate mean ± SEM, and n > 140 for each case.