Apoptosis and autophagy induction of Seleno-β-lactoglobulin (Se-β-Lg) on hepatocellular carcinoma cells lines

Abstract

β-lactoglobulin is important fraction in bovine milk. Selenium is an essential nutrient element. The apoptosis and autophagy induction of Se-β-Lg combined selenic acid in β-lactoglobulin on Hep G2 and Hep 3B cells were investigated in this study. MTT assay showed Se-β-Lg inhibited cells viability. Annexin V-FITC/PI and PI staining indicated Se-β-Lg triggered cells apoptosis and cell cycle arrest. Western blot of caspase-cascade suggested Hep G2 and Hep 3B cells occurred irreversible extrinsic apoptosis. TEM and protein expression of LC3 indicated Se-β-Lg induced cells autophagy. Further explore found Se-β-Lg induced up-regulation of p53 and Fas/FasL in Hep G2 cells. Simultaneously, N-acetyl-L-cysteine, pifithrin-α, Z-VAD-FMK and 3-MA were used. These results further demonstrated Se-β-Lg triggered autophagy and receptor-related apoptosis via p53-mediated Fas/FasL pathway in Hep G2 cells and induced autophagy and p53/Fas-independent caspase activation in Hep 3B cells. Our research revealed that Se-β-Lg had potential to act as chemopreventive compounds in HCC therapy.

Keywords

• Seleno-β-lactoglobulin
• Hepatocellular carcinoma cells lines
• Autophagy
• Apoptosis pathway
• p53