Apigenin inhibits glioma cell growth through promoting microRNA-16 and suppression of BCL-2 and nuclear factor-κB/MMP-9

Abstract

The present study aimed to investigate the effect of apigenin on glioma cells and to explore its potential mechanism. U87 human glioma cells treated with apigenin were used in the current study. Cell Counting Kit-8 solution and Annexin V-fluorescein isothiocyanate/propidium iodide Apoptosis Detection kit were used to analyze the effect of apigenin on U87 cell viability and apoptotic cell death. Reverse transcription-quantitative polymerase chain reaction analysis was also used to determine microRNA-16 (miR-16) and MMP-9 gene expression levels. Nuclear factor-κB (NF-κB) and B-cell CLL/lymphoma 2 (BCL2) protein expression levels were determined using western blot analysis. An anti-miR-16 plasmid was constructed and transfected into U87 cells. The current study demonstrated that apigenin significantly decreased cell viability and induced apoptotic cell death of U87 cells in a dose-dependent manner. Additionally, it was demonstrated that apigenin significantly increased miR-16 levels, suppressed BCL2 protein expression and suppressed the NF-κB/MMP9 signaling pathway in U87 cells. Furthermore, downregulation of miR-16 using the anti-miR-16 plasmid reversed the effect of apigenin on cell viability, BCL2 protein expression and the NF-κB/MMP-9 pathway in U87 cells. The results of the present study suggested that apigenin inhibits glioma cell growth through promoting miR-16 and suppression of BCL2 and NF-κB/MMP-9. In conclusion, the present study demonstrated the potential anticancer effects of apigenin on glioma cells.