Norepinephrine enhances cell viability and invasion, and inhibits apoptosis of pancreatic cancer cells in a notch-1-dependent manner

Pancreatic ductal adenocarcinoma (PDAC) is one of the most aggressive types of cancer, which is associated with a poor prognosis due to complexities in prevention, early diagnosis and effective treatment. The lack of understanding regarding its induction and specific pro-cancer mechanisms may contribute to its poor prognosis. The Notch-1 pathway is widely considered to be a critical tumor-promoting factor in PDAC. Previous studies have indicated that chronic psychological stress may promote the development of PDAC partially via the main downstream stress hormone, norepinephrine (NE); however, to the best of our knowledge, the role of the Notch-1 pathway in this process has not been studied. Therefore, the present study aimed to explore this process. The expression levels of Notch-1 pathway-associated molecules were measured in response to NE using reverse transcription-quantitative polymerase chain reaction and western blotting. Alongside NE treatment, two Notch-1 pathway blockers, Notch-1-specific small interfering (si)RNA and DAPT (an inhibitor of the Notch-1 pathway), were used to explore the relationship between NE and the Notch-1 pathway in the development of pancreatic cell malignant biological behaviors, including cell viability, apoptosis and cell invasion. The results demonstrated that treatment with NE enhanced cell viability and invasion, and inhibited apoptosis of PDAC cells; however, these effects were suppressed following treatment with Notch-1-specific siRNA and DAPT. In conclusion, NE may enhance the malignant biological behaviors of PDAC via activating the Notch-1 pathway.