The role of casticin in the apoptosis of pancreatic cancer cells and its mechanism

Objective: To investigate the function of casticin in the apoptosis of pancreatic cancer cells, and its possible mechanism. Methods: The proliferation of pancreatic cancer Miapaca-2 and Panc1 cells treated with 0, 10, 20, 30 and 40 μmol/L casticin for 24, 48 and 72 h was detected by CCK-8 assay. The effects of 0, 10, 20 and 30 μmol/L casticin on the colony formation, apoptosis and the expressions of cleaved caspase-3, cleaved caspase-9, cleaved poly ADP-ribose polymerase (PARP), phosphorylated phosphatidylinositol-3-kinase (p-PI3K) and phosphorylated protein kinase B (p-PKB, p-AKT) in pancreatic cancer Miapaca-2 and Panc1 cells were measured by colony formation assay, FCM and Western blotting, respectively.  Results: The 0, 10, 20, 30 and 40 μmol/L casticin could inhibit the proliferation of human pancreatic cancer Miapaca-2 and Panc1 cells in a dose- and time-dependent manner (all P < 0.05). The colony formation of Miapaca-2 and Panc1 cells was inhibited by casticin (all P < 0.01)，and it could also promote apoptosis in Miapaca-2 and Panc1 cells (all P < 0.05). After treatment with casticin, the expression levels of cleaved caspase-3, cleaved caspase -9 and cleaved PARP in Miapaca-2 and Panc1 cells were remarkably up-regulated (all P < 0.05), while the expression levels of p-PI3K and p-Akt were down-regulated (all P < 0.01). Conclusion: Casticin can inhibit the proliferation of pancreatic cancer cells, and promote the apoptosis. This effect may be related with the regulation of casticin on the expression levels of proteins which are involved in the mitochondria-dependent apoptosis. DOI:10.3781/j.issn.1000-7431.2017.11.521