Research Paper Volume 13, Issue 1 pp 1017—1031

Figure 5. AIM2 inhibits HCT116 cell proliferation, migration and EMT progress in a Gli1-dependent manner. (A) Colony formation assays to test viability of HCT116 cells stably transfected with empty vector (VEC) or plasmid encoding human AIM2 (AIM2) with or without Gli1 siRNA treatment. Quantitative analysis results were presented as the mean±SEM (n=3). (B) Transwell assays to test migration ability of HCT116 cells stably transfected with empty vector (VEC) or plasmid encoding human AIM2 (AIM2) with or without Gli1 siRNA treatment. Quantitative analysis results were presented as the mean±SEM (n=3). (C) Western blots of E-cadherin and Vimentin protein expression in HCT116 cells stably transfected with empty vector (VEC) or plasmid encoding human AIM2 (AIM2) in the presence or absence of Gli1 siRNA. GAPDH as a loading control. Each experiment was performed at least triplicate and the bands were quantified and presented as the mean±SEM. (D) Western blots of Gli1 protein expression in LoVo (VEC vs. AIM2) cells transfected with plasmids encoding human Gli1 or empty vector. (E, F) Colony formation assay (E) and transwell assay in LoVo (VEC vs. AIM2) cells transfected with plasmids encoding human Gli1 or empty vector. N, nonsignificant, *P<0.05, **P<0.01, based on a two-tailed paired Student’s t-test or ANOVA.