Selenious-β-lactoglobulin induces the apoptosis of human lung cancer A549 cells via an intrinsic mitochondrial pathway
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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.
KeywordsSelenious-β-lactoglobulin (se-β-lg) Antitumor activity Mitochondrial pathway
This study was funded by National Natural Science Foundation of China (No. 31271975).
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Conflict of interest
All authors declare that they have no conflict of interest.
Human and animal rights
This article does not contain any studies with human participants or animals performed by any of the authors.
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