Abstract:ObjectiveTo explore the effect and mechanism of celastrol on the proliferation, invasion and migration of non-small cell lung cancer (NSCLC)A549 cells. Methods After different concentrations of celastrol were used to treat NSCLC A549 cells, CCK-8 assay was used to detect cell proliferation inhibition and half inhibition rate (IC50); the morphology of A549 cells was observed by microscope; the colony formation ability of A549 cells was detected by plate cloning assay; the apoptosis rate of A549 cells was detected by Annexin V/PI double-staining flow cytometry; the invasion and migration ability of A549 cells were detected by Transwell assay and scratch assay; western blot was used to detect the changes of COX-2, MMP-2, MMP-9, p-p65, p65 protein expressions; RT-qPCR experiments were used to detect the changes of COX-2 mRNA, MMP-2 mRNA, MMP-9 mRNA expression. Results Celastrol inhibited the cell viability of A549 cells (P<0.05), and the 48 h IC50 was (2.607±0.163) μmol/L. After A549 cells was treated with celastrol, the cell number was significantly reduced, the cells were shrinked and round, the cell adhesion ability was weakened, the cell spacing becomeed larger, and the cell filopodia were reduced. Celastrol significantly inhibited the colony forming ability of A549 cells (P<0.05); celastrol significantly induced A549 apoptosis (P<0.05); celastrol significantly inhibited the invasion and migration ability of A549 cells (P<0.05); celastrol significantly inhibited COX-2 protein, MMP-2 protein, MMP-9 protein and p-p65/p65 in A549 cells expression(P<0.05); celastrol significantly inhibited the expression of COX-2 mRNA, MMP-2 mRNA and MMP-9 mRNA in A549 cells(P<0.05). Conclusions Celastrol can inhibit the proliferation, invasion and migration of NSCLC A549 cells, which may be related to the downregulation of COX-2, MMP-2, MMP-9 protein and mRNA expression through NF-κB signaling.