B-L Ji1, L-P Xia, F-X Zhou, G-Z Mao, L-X Xu. 1. Department of Laboratory Medicine, Hospital of Traditional Chinese Medicine of Lishui City, Lishui, Zhejiang, China. xulixia086@sina.com.
Abstract
OBJECTIVE: Pancreatic cancer is one of the leading causes of death from cancer in European countries and the United States. This study sought to investigate the effects of aconitine, a well-known aconitum plant-produced toxin, on pancreatic cancer cell growth and apoptosis and to explore the potential mechanisms. MATERIALS AND METHODS: In this study, pancreatic cancer cell lines Miacapa-2 and PANC-1 were cultured, and cell viability was examined in these two cells treated with different doses of aconitine. Moreover, cell apoptosis was also analyzed upon aconitine treatment, and the specific mechanism was examined by Western blot assay and caspase activity detection. RESULTS: The results showed that aconitine inhibited pancreatic cancer cell growth in a dose- and time-dependent manner. The administration of aconitine in Miapaca-2 and PANC-1 cells also induced cell apoptosis by upregulating the expression of pro-apoptotic factors Bax, cl-caspase-3, cl-caspase-9, and cleaved poly (ADP-ribose) polymerase 1 (PARP1), and by decreasing the anti-apoptotic Bcl-2 expression. More importantly, NF-κB was also decreased upon aconitine treatment. In a xenograft mouse model of pancreatic cancer, aconitine suppressed tumor growth and increased cell apoptosis. CONCLUSIONS: This study is the first report on the effects of aconitine on pancreatic cancer, and it reveals that aconitine may serve as a potent therapeutic strategy for clinical treatment of pancreatic cancer.
OBJECTIVE:Pancreatic cancer is one of the leading causes of death from cancer in European countries and the United States. This study sought to investigate the effects of aconitine, a well-known aconitum plant-produced toxin, on pancreatic cancer cell growth and apoptosis and to explore the potential mechanisms. MATERIALS AND METHODS: In this study, pancreatic cancer cell lines Miacapa-2 and PANC-1 were cultured, and cell viability was examined in these two cells treated with different doses of aconitine. Moreover, cell apoptosis was also analyzed upon aconitine treatment, and the specific mechanism was examined by Western blot assay and caspase activity detection. RESULTS: The results showed that aconitine inhibited pancreatic cancer cell growth in a dose- and time-dependent manner. The administration of aconitine in Miapaca-2 and PANC-1 cells also induced cell apoptosis by upregulating the expression of pro-apoptotic factors Bax, cl-caspase-3, cl-caspase-9, and cleaved poly (ADP-ribose) polymerase 1 (PARP1), and by decreasing the anti-apoptotic Bcl-2 expression. More importantly, NF-κB was also decreased upon aconitine treatment. In a xenograft mouse model of pancreatic cancer, aconitine suppressed tumor growth and increased cell apoptosis. CONCLUSIONS: This study is the first report on the effects of aconitine on pancreatic cancer, and it reveals that aconitine may serve as a potent therapeutic strategy for clinical treatment of pancreatic cancer.