In summary, as illustrated in Figure 9, we have identified a novel function for CtBP2 as a transcription co-repressor that interacts with SNAI1 and contributes to inducing the EMT phenotype of HCC cells. We found that GLI1 upregulated both SNAI1 and CtBP2. This upregulation results in the induction of EMT, and, therefore, this study characterizes the mechanism by which GLI1 modulates the EMT in HCC. Finally, CtBP2 appears to be an effective predictive factor for HCC outcome after liver resection and additional future studies developing CtBP2 as a prognostic marker, in addition to studies investigating its potential as an HCC treatment target, should be conducted.
