Objective:　　To investigate the expression of Forkhead Box C2(FOXC2) in pancreatic cancer and its effects on invasion and metastasis of pancreatic cancer cells.　　Methods：　　Immunohistochemistry and real-time PCR were used to detect the protein and mRNA expressions of FOXC2 in 112 cases of pancreatic cancer tissues. FOXC2 were over-expressed by using the technology of lentiviral transfection in BXPC3 and MiaPaCa2 pancreatic cancer cell lines. FOXC2 were knocked down by using the technology of RNA interference(RNAi) in BXPC3 and MiaPaCa2 pancreatic cancer cell lines. Chamber assay was used to examine the cell migration ability. The nude mouse tumor metastasis model was constructed to detect the influence of FOXC2 on invasion and metastasis in pancreatic cancer cells. Western-blot method was used to detect the expression differences of epithelial-mesenchymal transition related proteins (N-cadherin, Vimentin and Snail) in these cell lines. Co-immunoprecipitation and Western-blot methods were used to detect the interaction between FOXC2 and IGF2BP3.　　Results：　　FOXC2 protein and mRNA were up-regulated in paired pancreatic cancer tissues(P<0.01). FOXC2 protein was closely related to patients’ T stage(P<0.05), TNM stage(P<0.01) and lymph node metastasis(P<0.01). The protein expression of FOXC2 is higher in advanced stage of the tumor(P<0.01). There was no significant difference in the expression level of FOXC2 in terms of gender, age, nerve metastasis and vascular invasion(P>0.05). The expression level of FOXC2 in pancreatic cancer cell lines which were transfected by FOXC2 over-expression vector was up-regulated. The expression level of FOXC2 in pancreatic cancer cell lines which were transfected by FOXC2 shRNA lentiviral vector was down-regulated. The colony-forming ability of FOXC2 over-expressed cell line was significantly increased(P<0.01), and the　　colony-forming ability of FOXC2 low-expressed cell line was significantly reduced(P<0.01). Through constructing the nude mouse tumor metastasis model, we proved the invasion and metastasis ability of pancreatic cancer cells were decreased after down-regulating FOXC2. Silencing FOXC2 could down-regulated the expression of N-cadherin, Vimentin and Snail. FOXC2 interacts with IGF2BP3 in pancreatic cancer cells.　　Conclusion：　　FOXC2 is highly expressed in pancreatic cancer and promotes EMT, invasion and metastasis of pancreatic cancer cells by interacting with IGF2BP3. FOXC2 may serve as a new target for the treatment of pancreatic cancer.