TRIM11 Regulates β-Catenin Pathway in vitro and in vivo To explore the underlying mechanism by which TRIM11 regulates gastric cancer, we did some literature research and found that several TRIM proteins can regulate β-catenin pathway, so we hypothesize that TRIM11 may regulate GC through β-catenin pathway. We detected the expression level of β-catenin in TRIM11 overexpression in MGC-803 cells and found that it was increased. Then, we further investigated the expression level of β-catenin downstream molecules and found that CyclinD1 and C-myc were upregulated and Axin2 were downregulated (Figure 6A) in overexpression of TRIM11 in MGC-803 cells, while knockdown of TRIM11 in HGC-27 cells displayed the opposite results (Figure 6B). We also found that the protein level of β-catenin in shTRIM11 xenograft tumors was significantly lower than that of shNC xenograft tumors (Figure 6C). What is more, we also analyzed the protein level of β-catenin in cell nucleus and cytoplasm by Western blotting and Immunofluorescence. Results show that overexpression of TRIM11 promotes the transfer of β-catenin protein from cytoplasm to nucleus (Figure 6D and E). These data suggest that TRIM11 may exert its oncogenic effect through β-catenin pathway.