To further study the role of CtBP2 in HCC progression, we conducted HCC xenograft experiments in nude mice. Huh7 CtBP2 and Huh7 Vector cells were subcutaneously injected into six nude mice. The growth of xenograft tumors was observed weekly using calipers and tumors were harvested after four weeks. The xenograft tumors derived from the Huh7 CtBP2 cells (Huh7 CtBP2 Group) were notably larger than those derived from the Huh7 Vector cells (Huh7 Vector Group) (Figure 7A). Unpaired Student's t-tests confirmed that the xenograft tumors obtained from the Huh7 CtBP2 Group were remarkably larger than the tumors obtained from the Huh7 Vector Group ( p = 0.001, Figure 7B). IHC staining demonstrated significantly stronger N-cadherin expression and less E-cadherin expression in the Huh7 CtBP2 Group's xenograft tumors (Figure 8). We did not observe upregulation of either GLI1 or SNAI1 in the Huh7 CtBP2 Group, providing evidence that CtBP2 did not mediate either GLI1 or SNAI1 expression in xenograft HCC tumors. In summary, these results supported the hypothesis that CtBP2 promotes tumor progression and induces the EMT phenotype in HCC.
