Casticin induces apoptosis and mitotic arrest in pancreatic carcinoma PANC-1 cells

Pancreatic cancer is one of the most malignant tumors that responded poorly to currently available chemotherapy. Casticin, a flavonoid compound, has been reported to induce apoptosis in various cancer cell lines. However, there is no report on the anti-pancreatic cancer potential of casticin. In the present study, we showed for the first time that casticin strongly inhibits the growth of PANC-1 pancreatic carcinoma cells. The anti-proliferative effect assessed by 3-(4,5-Dimethylthiazol-2-yl)-2,5-Diphenyltetrazolium Bromide (MTT) assay demonstrated that casticin inhibited the growth of PANC-1 cells in a dose-dependent manner. Further analysis using flow cytometry and immunoblot showed that the growth inhibitory effect of casticin was associated with cell cycle arrest at G2/M phase and induction of apoptosis. Mechanistic studies indicated that the induction of apoptosis was associated with up-regulation of pro-apoptotic protein Bax, down-regulation of anti-apoptotice protein Bcl-2 and activation of caspase-3. These findings suggest that casticin may be a promising candidate for treating human pancreatic cancer.   Key words: Casticin, PANC-1, apoptosis, G2/M phase arrest, caspase-3.