Abstract

Significant progress has been made in the management of non-small cell lung cancer (NSCLC), though a big barrier remains, which is epithelial–mesenchymal transition (EMT). Our study aimed to evaluate the function of miR-6884-5p and S100A16 in EMT-aggravated NSCLC. The tumor tissues and adjacent tissues from 92 NSCLC patients were collected to analyze the expression of miR-6884-5p and S100A16. Then lung cancer cell line A549 was co-transfected with miR-6884-5p mimics and S100A16 to further evaluate their function. Compared to adjacent tissues, low expression of miR-6884-5p was observed in the NSCLC tissues and associated with severe NSCLC progression. MiR-6884-5p expression was negatively correlated with EMT in NSCLC. Luciferase assay data revealed that miR-6884-5p could directly bind to the 3’UTR of S100A16 and inhibited the expression of S100A16 in A549 cells. Moreover, miR-6884-5p mimics significantly ameliorated EMT progression, and overexpression of S100A16 could reverse the inhibitory effect of miR-6884-5p in A549 cells. MiR-6884-5p inhibited EMT through directly targeting S100A16 in NSCLC. Our findings suggest that miR-6884-5p could be a diagnostic marker of NSCLC, as well as a potential candidate for NSCLC treatment.