Abstract: Objective To explore the influence of miRNA-223 （miR-223） on drugresistance of nonsmall cell lung cancer A549／DDP cells to dichorodiamine platinum （DDP） and its possible mechanism. Methods The real-time fluorescence quantitative PCR （qRT-PCR） was used to measure the miR223 level of A549／DDP cells. According to the experimental protocol， A549／DDP cells were divided into 3 groups： control group， empty vector transfection group （cells transfected with unrelated sequence） and inhibitor group （cells transfected with miR-223 inhibitor）. The qRT-PCR and CCK-8 were applied to detect the effect of transfection and proliferation at 24， 48， 72 and 96 h posttransfection. The changes of drugresistance of A549／DDP cells to cisplatin were measured by CCK-8. The cell cycle and apoptosis at 48 h posttransfection were detected via flow cytometry. The changes of expression of multidrug resistance protein， such as P-glycoprotein （P-gp）， multidrug resistance associated protein 1 （MRP1） and lung resistance related protein （LRP）， were evaluated by Western blotting. Results A higher level of miR-223 was observed in A549／DDP cells than in A549 cells with a （7.14±0.26）fold increase. There was a decreased miR-223 level in inhibitor group after transfection， which was further decreased compared to （67.15±2.84）％ of the control group and （65.80±3.47）％ of the empty vector transfected group at 96 h posttransfection （P＜0.05）. Compared with the control group， there were elevated inhibitory rates of proliferation， early and late apoptotic rates and proportion of cells in G0／G1 phase but reduced proportion of cells in S and G2／M phases and three protein levels related to resistance genes in inhibitor group. The inhibited concentration of 50％ （IC50） for DDP was （15.67±1.30） μg／ml in inhibitor group， lower than （33.71±2.61） μg／ml in control group. Conclusion MiR-223 can increase the drug resistance of A549／DDP cells to DDP， possibly by increasing the gene expression related to resistance. The reduced level of miR223 resulted in the inhibition of the proliferation, induction of apoptosis and cell cycle arrest and the downregulation of drug resistance protein.