Luteolin inhibits proliferation of lung cancer A549 cells by increasing ROS production and inhibiting the AKT/mTOR signaling pathway and HO-1 expression
Objective To investigate the mechanism of luteolin for inhibiting proliferation of lung cancer A549 cells.Methods A549 cells treated with different concentrations of luteolin for 48 h were evaluated for changes in cell viability,proliferation,reactive oxygen species(ROS)production and apoptosis using MTT assay,plate cloning assay,EdU staining,DCFH-DA assay and Hoechst33258 staining.The changes in cell autophagy were examined with MDC staining,and the expressions of apoptosis-related proteins(Bax,Bcl-2,and cleaved caspase-9),autophagy-related proteins(LC3B,Beclin 1,and P62),AKT/mTOR pathway proteins,and HO-1 protein were detected using Western blotting.Results Treatment with luteolin dose-dependently inhibited the viability and proliferation of A549 cells,increased intracellular ROS levels,up-regulated the expressions of Bax,cleaved caspase-9,and Beclin 1,increased the LC3B-Ⅱ/LC3B-Ⅰ ratio,down-regulated the expressions of Bcl-2 and P62,and induced cell apoptosis and autophagy.Luteolin also significantly inhibited the phosphorylation of AKT and mTOR and down-regulated the expression of HO-1 protein in the cells.Conclusion Luteolin induces apoptosis and autophagy to inhibit proliferation of A549 cells by increasing ROS production,inhibiting the AKT/mTOR pathway and down-regulating HO-1 protein expression.
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