Fentanyl inhibits cell viability in human pancreatic cancer cell line and tumor growth in pancreatic cancer cell-transplanted mice.

Pancreatic cancer is a kind of devastating disease with a high mortality rate. Fentanyl has been widely applied to anesthesia and analgesia in pancreatic cancer therapy, and is also demonstrated to inhibit the growth of some kinds of cancer cells in existed studies. To investigate the functions of fentanyl in pancreatic cancer, we conducted a series of in vivo and in vitro experiments using human pancreatic cancer cells SW1990 and fentanyl treatment. The cells were transplanted to BALB/c nude mice to generate pancreatic tumor for monitoring tumor growth. Viability, apoptosis, migration and invasion, and cell cycle of SW1990 cells were also analyzed. To reveal the functional mechanisms of fentanyl, the expression changes of factors in these cellular activities were detected. Results showed a significant inhibition of pancreatic tumor growth in the fentanyl-treated group. Fentanyl also inhibited viability of SW1990 cells in vitro. Detailed results showed fentanyl led to promoted cell apoptosis via arresting cells in G0/G1 phase. It also suppressed cell migration and invasion. Further proofs indicated that the factors related to cell apoptosis (Bcl-2, p53 and Caspase-3), cell cycle (p21, Cyclin D1 and CDK4) and epithelial-mesenchymal transition (E-cadherin, Vimentin and α-SMA) showed the corresponding expression changes. Fentanyl might execute its functions via the suppressed MAPK pathways, since the key factors, p38, ERK1/2 and JNK were all down-regulated by fentanyl. This study indicated fentanyl could inhibit viability and growth of pancreatic cancer cells, providing a possible strategy for pancreatic cancer treatment.