Effect And Mechanism Of Apigenin On Migration And Invasion Of Human Lung Cancer A549Cells

Objective To evaluate whether apigenin can inhibits cell migration, invasion and itsunderlying mechanisms in human lung cancer cell line A549.Methods A549cellswere cultured with different concentrations of apigenin for24hours, and CCK8assaywas used to evaluate the cell inhibition rates. According to the results of the proliferationinhibition, the cells treated with appropriate concentration of AP were used for the next experiment.Cells migration and invasion capabilities were evaluated by means of transwell andtranswell matrix penetration assays. The activitis and expressions of invasion-relatedproteins matrix-metallopeptidase2(MMP-2) and vascular endothelial growth factor(VEGF) were analyzed by enzyme-linked immunosorbent assay (ELISA) and Westernblotting. Results Apigenin causes concentration-dependent inhibition of theproliferation of A549cells. The cell viability was more than75%in0-20μmol/L,wichshows unconspicuous inhibiting effect.The half inhibitory concentration for24h was46．5±3.7μmol/L. As the concentration of drug intervention,20μmol/L group (noobvious inhibition of cell proliferation) and40μmol/L group(significant inhibition of cellproliferation) were selected for the migration and invasion experiment.The migration andinvasion capabilities of A549cells treated with apigenin were significantlydecreased,especially in the40μmol/L group. ELISA and Western blotting demonstratedthat the protein activitis and expressions of MMP-2and VEGF were suppressed byapigenin in A549cells. Conclusion: Apigenin may play its role inhibiting lung cancercell line A549migration and invasion via suppression the expressions of MMP-2andVEGF.