Fig. 4: MACC1 employs S100A4 through β-catenin signaling to drive cancer cell motility.

MACC1-specific cell motility depends on S100A4. Overexpression of MACC1 in HCT116 cells induced transwell migration, but not in S100A4-KO counterparts (A). MACC1-induced cell migration in HCT116 and SW480 cells, and this effect was reverted by niclosamide, a transcriptional inhibitor of S100A4 (B, C). MACC1 increased S100A4 in presence of DMSO, and three independent β-catenin inhibitors (niclosamide, FH535 and LF3) largely reversed this upregulation on mRNA and protein level to expression levels of HCT116/vector cells (D). Numeric results shown as means ± SEM of 3 independent experiments, test for significance with Student’s t-test, or ANOVA and Tukey correction for multiple testing.