Glioma-associated oncogene 1 (GLI1) is a downstream transcription factor in the hedgehog signaling pathway that reportedly accelerates the progression of various cancers, including basal cell carcinoma [16], colon cancer [17], medulloblastoma [18], gastric cancer [19] and pancreatic carcinoma [20]. We previously reported GLI1 overexpression in HCC tissues and were able to predict rapid tumor recurrence after surgery using GLI1 expression levels. GLI1 consists of a conserved C2H2 zinc finger DNA-binding domain that specifically interacts with a GACCACCCA-like motif in the promoters of various target genes. GLI1 mediates the expression of a variety of important cancer progression genes, including SNAI1 [21], ABCG2 [22], CYLD, DNMT [23], RegIV [24], AKT [25] and Caveolin-1 [26]. We demonstrated that aberrantly upregulated GLI1 promoted HCC progression by regulating epithelial-mesenchymal transition (EMT) through the GLI1 transcriptional target Snail Family Zinc Finger 1 (SNAI1) [21]. We found seven potential GLI1 binding sites in the CtBP2 promoter, which lead us to hypothesize that GLI1 overexpression might contribute to the upregulation of CtBP2 in HCC.
