Abstract: Objective　To investigate the functional role and mechanism of miR-208a on proliferation, invasion and migration of non-small cell lung cancer (NSCLC) A549 cells. Methods　(1) A549 cells were transfected with miR-208a mimic, NC mimic, miR-208a inhibitor and NC inhibitor, respectively, and the overexpression and interference efficiency of miR-208a were detected by quantitative polymerase chain reaction (qPCR). CCK-8, Transwell and wound healing assays were used to evaluate the effects of miR-208a on proliferation, invasion and migration of A549 cells. Bioinformatics websites such as miRDB, PicTar, Targetscan and miRanda were used to predict the downstream target genes of miR-208a. PTPRG 3'UTR wild-type and mutant double luciferase reporter gene vectors were constructed and co-transfected with miR-208a into HEK-293T cells to observe the changes of luciferase activity. (2) A549 cells in logarithmic phase were taken, and negative control group (si-NC group), PTPRG knockdown group (si-PTPRG group), PTPRG knockdown group + miR-208a interference group (si-PTPRG + miR-208a inhibitor group) were set up. CCK-8, Transwell test and scratch test were used to detect the effects of PTPRG on proliferation, invasion and migration of A549 cells. qPCR and Western blot assays were performed to detect the expression levels of PTPRG mRNA and protein. Results　There were increased levels of miR-208a mRNA expression, cell proliferation, migration and invasion in miR-208a mimic group compared with those of NC mimic group (P＜0.05). By contrast, miR-208a inhibition exerted the opposite effects. Bioinformatics analysis showed that PTPRG was the target gene of miR-208a, and the overexpression of miR-208a could reduce the luciferase activity of PTPRG 3'UTR wild-type, and miR-208a inhibitor could increase the luciferase activity of PTPRG 3'UTR wild-type, indicating that miR-208a could bind to the 3'UTR sequence of PTPRG. Further studies showed that compared with si-NC group, the proliferation, invasion and migration of cells were significantly increased in si-PTPRG group, and the expression levels of PTPRG gene and protein were decreased (P＜0.05). Compared with si-PTPRG group, the proliferation, invasion and migration ability were decreased in si-PTPRG + miR-208a inhibitor group, and the expression levels of PTPRG gene and protein were increased. Conclusion　miR-208a promotes the proliferation, invasion and migration of A549 cells by targeting PTPRG.

Key words: carcinoma, non-small-cell lung, A549 cells, receptor-like protein tyrosine phosphatases, microRNAs, cell proliferation, cell movement ；miR-208a