Background and purpose: MicroRNA (miRNA) belongs to a class of 19 to 30 nucleotidelong

endogenous noncoding RNA expressed in eukaryotes and predominantly inhibits gene expression at the posttranscriptional level. The miRNAs play critical roles in cell proliferation and differentiation

apoptosis

metabolism

and immune regulation. This study aimed to detect the expression of miR-216a-5p in lung cancer tissues and lung cancer cell lines

and to discuss the effects of miR-216a-5p on the invasion ability of lung cancer cells and the mechanism. Methods: Quantitative real-time PCR (qRT-PCR) was used to detect the expression of miR-216a-5p in lung cancer tissues of 55 cases and 7 lung cancer cell lines. Three lung cancer cell lines of A549

95D and H460 were transiently transfected by miR-216a-5p

and Transwell was used to detect the effects of miR-216a-5p on the invasion of lung cancer cell lines. The dual luciferase reporter plasmids containing the miR-216a-5p candidate target gene and the gene of matrix metalloproteinase 16 (MMP16) were predicted and constructed. qRT-PCR and Western blot were used to detect the changes in mRNA and protein levels of target gene MMP16 by miR-216a-5p. The interference of MMP16 by siRNA and up-regulation miR-216a-5p by transfection were compared on the invasion of lung cancer cells. Results: The miR-216a-5p expression levels were all significantly reduced in 90.91% (50 of 55 patients) tumor tissues compared with corresponding adjacent normal lung tissues (P0.05). The miR-216a-5p expression levels were only 7.00%-32.00% in 7 lung cancer cells compared with the control group (P0.05). Up-regulation of the expression of miR-216a-5p inhibited the invasion of lung cancer cells; interference of MMP16 by siRNA

as well as up-regulating miR-216a-5p by transfection

inhibited the expression of MMP16 in lung cancer leading to inhibition of the invasion of lung cancer cells. Conclusion: miR-216a-5p can be a candidate marker in clinical diagnosis and it can inhibit the invasion of lung cancer cells by down-regulating the expression of MMP16.