promotes pancreatic cancer cell proliferation, invasion and migration via activation of the signaling pathway.

The biological functions of neuropilin and tolloid-like 2 () in the progression of pancreatic cancer remained unexplored. We aimed to investigate the biological roles and underlying molecular mechanisms of in pancreatic cancer. Thirty paired pancreatic tumor tissue samples and corresponding nontumor tissues were obtained from 30 pancreatic cancer patients who did not receive preoperative chemotherapy or radiotherapy. The changes in multiple cellular functions associated with tumor progression were assessed after knockdown/overexpression in pancreatic cancer cell lines. Additionally, a mouse-xenograft model was developed to verify the in vitro results. was upregulated in pancreatic tumor tissues. Elevated expression of was not only associated with an advanced tumor stage, but was also a prediction of poor prognosis for pancreatic cancer patients. Knockdown of in pancreatic cancer cell lines arrested the cell cycle and inhibited cell proliferation, colony formation, invasion, and migration; in contrast, overexpression of had an opposite effect on all of these parameters. A specific inhibitor, cryptotanshinone, reversed the tumor-promoting effects induced by overexpression in pancreatic cancer. Western blot analysis showed that invasion and migration were closely related to epithelial-mesenchymal transition, and that the signaling pathway was involved in -mediated oncogenic transformation in pancreatic cancer cells. Furthermore, knockdown significantly inhibited the growth of pancreatic tumor xenografts in nude mice. has an important role in the progression and metastasis of pancreatic cancer and could serve as a novel candidate for targeted therapy of pancreatic cancer.