Effect of casticin on the proliferation and apoptosis of hepatocellular carcinoma cells via regulating PI3K/AKT pathway
Objective:To investigate the effect and mechanism of casticin on the proliferation and apoptosis of hepatocellular carcinoma cells via regulating phosphatidylinositol-3-kinase(PI3K)/protein kinase B(AKT)pathway.Methods:HepG2 and Hep3B hepatocellular carcinoma cell lines were cultured and divided into control group,different concentrations of casticin(10,20,40,80 μmol/L)group,solvent control(DMSO with volume fraction of 0.1%)group,solvent +40 μmol/L casticin group,AKT agonist SC-79(5 μmol/L)+40 μmol/L casticin group.After 48 hours of treatment,cell viability,cell clone count,cell apoptosis rate,and expression levels of B cell lymphoma-2(Bcl-2),cytochrome C(CytC),Bcl-2 associated X protein(Bax),cleaved caspase-3,phosphorylated PI3K(p-PI3K),and phosphorylated AKT(p-AKT)were detected.Results:The 10,20,40 μmol/L vitexin reduced the cell viability of HepG2 and Hep3B on a concentration dependent manner.The cell clone numbers,the expression levels of Bcl-2,CytC,p-PI3K,p-AKT in HepG2 and Hep3B of 40 μmol/L casticin group were lower than those of the control group,while the expression levels of Bax and Cleared caspase-3 were higher than those of the control group(P<0.05).The regulatory effect of 40 μmol/L casticin on HepG2 and Hep3B was weakened by AKT agonist SC-79.Conclusion:The casticin inhibits the proliferation of hepatocellular carcinoma cells by inhibiting the PI3K/AKT pathway.
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