Abstract: Abstract: Objective To investigate the inhibitory effects and mechanisms of a nature product derivate oridonin on in⁃ vasion of human lung cancer. Methods Human lung cancer A549 and PC-9 cell lines were treated with oridonin. MTS as⁃ say was used to determine cell proliferation. Transwell assay was used to determine the cell invasion, and adhesion assay to determine the cell adhesion. Flow cytometry was used to determine cell cycle. Western blotting and realtime-PCR were used to detect expression levels of CDK1, mTOR, p53, p21, E-cadherin, CD44, β-catenin, uPA, MMP-2/9, p-AKT and p-Src. The luciferase reporter assay was used to detect the NF-κB promoter activity. Results In vitro proliferation, invasion and adhesion of A549 and PC-9 cells were significantly inhibited by oridonin. The cell cycle was halted by G2/M phase, and ex⁃ pressions of E-cadherin, p53 and p21 were promoted, while expressions of CDK1, mTOR, CD44, β-catenin, uPA, MMP-2/ 9, p-AKT and p-Src and promoter activity of NF-κB were down-regulated. Conclusion Oridonin is able to inhibit the in vitro invasion of human lung cancer A549 and PC-9 cell lines, which might be correlated with its abilities to regulate the ty⁃ rosine kinase activity.

Key words: Rubescensine, lung neoplasms, neoplasm invasiveness, A549, PC-9