MicroRNA-629 promotes the tumorigenesis of non-small-cell lung cancer by targeting FOXO1 and activating PI3K/AKT pathway

OBJECTIVE MicroRNA-629 (miR-629) has been found to play an important role in the pathogenesis of human cancers. However, the function of miR-629 is still unknown in non-small-cell lung cancer (NSCLC). The purpose of this study is to preliminarily elucidate the regulatory mechanism of miR-629 in NSCLC. MATERIALS AND METHODS The mRNA and protein expression was measured by real-time quantitative polymerase chain reaction (RT-qPCR) and western blot analysis. The function of miR-629 was investigated by MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide) and Transwell assays. The relationship between miR-629 and FOXO1 was confirmed by dual luciferase assay. RESULTS MiR-629 was upregulated in NSCLC tissues and cells. High expression of miR-629 predicted poor prognosis in patients with NSCLC. Moreover, miR-629 promoted cell proliferation, migration and invasion in NSCLC cells. In addition, FOXO1 was confirmed as a direct target of miR-629 in NSCLC. Furthermore, knockdown of FOXO1 also promoted proliferation, migration and invasion of NSCLC cells. More importantly, overexpression of FOXO1 weakened the carcinogenesis of miR-629 in NSCLC. Besides that, miR-629 promoted EMT and activated the PI3K/AKT pathway in NSCLC. CONCLUSIONS MiR-629 promotes the progression of NSCLC by targeting FOXO1 and regulating EMT/PI3K/AKT pathway.