Methyl protodioscin induces G2/M cell cycle arrest and apoptosis in A549 human lung cancer cells

Background: Methyl protodioscin (MPD) is a furostanol bisglycoside with antitumor properties. It has been shown to reduce proliferation, cause cell cycle arrest. Objective: The present study elucidates the mechanism underlying MPD’s apoptotic effects, using the A549 human lung cancer cell line. Materials and Methods: The human pulmonary adenocarcinoma cell line A549 was obtained from the Cell Bank of the Animal Experiment Center, North School Region, Sun Yat‑Sen University. All of the cells were grown in RPMI 1640 supplemented with 10% fetal calf serum (Hyclone, Logan, UT, USA), penicillin (10,000 U/l), and streptomycin (100 mg/l) at 37°C in a 5% CO2 humidified atmosphere. The induction of apoptosis was observed in flow cytometry and fluorescent staining experiments. Results: MPD showed growth inhibitory effects in A549 cells in a dose‑ and time‑dependent manner. The significant G2/M cell cycle arrest and apoptotic effect were also seen in A549 cells treated with MPD. MPD‑induced apoptosis was accompanied by a significant reduction of mitochondrial membrane potential, release of mitochondrial cytochrome c to cytosol, activation of caspase‑3, downregulation of Bcl‑2, p‑Bad, and upregulation of Bax. Conclusion: Our results show that the induction of apoptosis by MPD involves multiple molecular pathways and strongly suggest that Bcl‑2 family proteins signaling pathways. In addition, mitochondrial membrane potential, mitochondrial cytochrome c and caspase‑3 were also closely associated with MPD‑induced apoptotic process in human A549 cells.