Abstract
In this study, the cytotoxic activity of selenious-β-lactoglobulin (Se-β-Lg) and the anticancer mechanism were investigated in human lung cancer A549 cells in vitro. MTT assay showed that Se-β-Lg at 200 μg/mL exhibited a significant suppression effect on A549 cells and the maximum inhibition rate reached 90% after 72 h treatment. Flow cytometry analysis revealed that 200 μg/mL of Se-β-Lg induced cell cycle arrest at G0/G1 phase. Cell apoptosis was induced via the generation of reactive oxygen species (ROS) and the decrease of mitochondrial membrane potential (ΔΨm) in a time-dependent manner. Furthermore, Se-β-Lg suppressed the expression of Bcl-2 and improved the level of Bax, leading to the release of cytochrome c and a higher expression of caspase-3 in A549 cells. In summary, Se-β-Lg could induce apoptosis in A549 cells via an intrinsic mitochondrial pathway and it might serve as a potential therapeutic agent for human lung cancer.