We report that CtBP2 expression was upregulated in the HCC tissues examined in this study, and that elevated CtBP2 expression was associated with elevated GLI1 expression and poor overall postsurgical survival. We verified that CtBP2 was directly upregulated by GLI1 in vitro, and demonstrated that the upregulated CtBP2 bound the PQDLSLK motif of SNAI1 in the nucleus. Additionally, the oncogenic Role of CtBP2 was validated using a HCC xenograft model. Therefore, the findings of this study indicate that CtBP2 might facilitate GLI1-SNAI1 induced EMT in HCC. This is the first report describing the mechanism underlying CtBP2 overexpression, identifying the role played by CtBP2 in EMT in HCC and showing CtBP2 is an effective predictive biomarker of patient outcome after HCC surgery.
