Abstract: Objective To investigate the expression of miR203 in lung adenocarcinoma and analyze the relationship between miR-203 and migration and invasion of lung adenocarcinoma cells. The involved molecular mechanisms are also initially explored. Methods miR-203 was detected in lung tissues of 40 patients with lung adenocarcinoma by real time PCR. The expression of miR-203 was detected in lung adenocarcinoma cell lines H1650， A549， H1975， SPC-A-1 by real time PCR. The potential target gene of miR203 was predicted by online bioinformatic softwares. Pre-miR-203 mimics， Bmi-1 gene and Bmi-1 siRNA were transfected into H1975 cell line by lipofectamine 2000. The Bmi-1 protein level was analyzed by Western blotting. The predicted miR-203 binding site in Bmi-1 3’untranslated region（UTR） was validated by dualluciferase reporter gene assay. The migration ability of H1975 cells was determined by Transwell assay.
Results The relative expression of miR-203 in lung adenocarcinoma tissues was 0.065±0.013. The expression level of miR-203 in the lymph node metastasis group was lower than those in the non-metastasis group. The relative expression of miR-203 in H1650, A549，H1975 and SPC-A-1 cell lines were 0.280±0.102，0.308±0.168，0.167±0.073 and 0.287±0.096， respectively. Bmi-1 was a potential target gene of miR-203 predicted by miRanda and TargetScan. The Bmi-1 protein level was remarkably decreased in the pre-miR-203 mimics group. Dual-luciferase reporter gene assay validated the predicted miR-203 binding site of Bmi-1 3’UTR. Overexpression of miR-203 significantly inhibited the migration and invasion of H1975 cells， whereas the cell migration and invasion ability could be restored by overexpression of Bmi-1. Conclusion miR-203 can suppress the migration of lung adenocarcinoma cell line H1975 via downregulating Bmi-1 expression. miR-203 might be a potential tumor metastasis suppressor miRNA.