Inhibitory effect of acacetin on nonsmall cell lung cancer A549 cells and its mechanism
YAN Qingtao1, WAN Siao1, LIU Yi1, LU Jian1,2, WU Zhan′ao3
（1. Institute of Life Science, Jiangsu University, Zhenjiang Jiangsu 212013; 2. School of Medicine, Jiangsu University, Zhenjiang Jiangsu 212013; 3. Department of Stomatology, Jinling Hospital, Medical School of Nanjing University, Nanjing Jiangsu 210093, China)
Abstract： Objective： To investigate the effect and molecular mechanisms of acacetin on migration, invasion and angiogenesis of non-small cell lung cancer (NSCLC) A549 cells. Methods: The effects of various concentrations of acacetin on A549 cell viability were detected by MTT assay and IC50 was calculated. The A549 cells were treated with various concentrations of acacetin, and the relative expression levels of vascular endothelial growth factor (VEGF), Ecadherin and matrix metalloproteinase-9 (MMP-9) were detected by Western blotting. And the ability of cell migration, invasion and angiogenesis was detected by scratch wound healing, Transwell, immunofluorescence and tubulogenesis tests, respectively. VEGF plasmid was overexpressed or knocked down in A549 cells, and the relative expression levels of VEGF, E-cadherin and MMP-9 were detected by Western blotting, and the ability of the migration, invasion and angiogenesis of the cells were further evaluated. Results: Compared with 0 μmol/L group, A549 cell viability in 10, 20, 30, 40 and 50 μmol/L acacetin groups was significantly decreased (P<0.01), and in a certain concentrationdependent manner, IC50 was 34-49 μmol/L. Compared with 0 μmol/L group, the migration, invasion and angiogenesis of A549 cells in 10, 20 and 40 μmol/L acacetin groups were significantly decreased (all P<0.05), and the expression levels of VEGF and MMP-9 protein were significantly decreased (all P<0.01), while the expression level of E-cadherin protein was significantly increased (P<0.01). Compared with blank control or overexpression negative control group, the expression level of MMP-9 protein in A549 cells in overexpression group was significantly increased, while the expression level of E-cadherin protein was significantly decreased, and the ability of cell migration, invasion and angiogenesis was significantly enhanced (all P<0.05). Compared with blank control or knockdown negative control group, the expression level of MMP-9 protein in A549 cells in knockdown group was significantly decreased, while the expression level of E-cadherin protein was significantly increased, and the ability of cell migration, invasion and angiogenesis was significantly decreased (all P<0.05). Conclusion: Acacetin may inhibit migration, invasion and angiogenesis of NSCLC A549 cells by decreasing VEGF expression.
