Suppression of CD26 inhibits growth and metastasis of pancreatic cancer.

CD26/DPPIV is a glycosylated transmembrane type II protein and has a multitude of biological functions, while its impact on the malignant phenotypes of cancer cells has not been fully understood. This study aimed to investigate the effect of CD26 on growth and metastasis of pancreatic cancer cells in vitro and in vivo. We found in this study that CD26 expression was higher in cell lines that derived from the metastatic sites than those from the primary tumor sites. In specimens of pancreatic cancer patients, CD26 expression was higher in cancerous tissues than in paired normal tissues. In in vitro experiments, knockdown of CD26 expression inhibited cell growth, migration, invasion, colony formation, and increased cell apoptosis of pancreatic cancer cells. Knockdown of CD26 also decreased tumor growth and liver metastasis in vivo by using xenograft animal models. Suppression of CD26 could inhibit expression of epithelial-mesenchymal transition (EMT) regulatory genes. Our results indicated that CD26 may represent a new therapeutic target for pancreatic cancer.