reversed GLI1/SNAI1 driven EMT, but CtBP2 could not induce EMT in HCC cells without SNAI1 expression. Interestingly, we found that enhanced GLI1 expression promoted CtBP2 upregulation. Fourteen potential GLI1-binding sites were observed in the CtBP2 promoter after searching the RCSB Protein Data Bank. ChIP and luciferase reporter assays suggested that GLI1 bound the −1350/−652 bp CtBP2 promoter fragment. These data indicated that GLI1 directly promoted CtBP2 expression. Therefore, we concluded that SNAI1 and CtBP2 both promoted the EMT phenotype of HCC cells, could directly interact with one another and were both directly upregulated by GLI1.
