microRNA-605 inhibits the oncogenicity of non-small-cell lung cancer by directly targeting Forkhead Box P1.

microRNA-605 (miR-605) is dysregulated in multiple cancers and plays crucial roles in regulating cancer progression. However, little is known about the expression pattern and detailed roles of miR-605 in non-small-cell lung cancer (NSCLC). Thus, in this study, we evaluated miR-605 expression in NSCLC along with its clinical significance. More importantly, the detailed roles and the underlying molecular mechanisms of miR-605 in NSCLC were explored. Quantitative reverse transcription polymerase chain reaction (RT-qPCR) was employed to detect miR-605 expression in NSCLC tissues and cell lines. A series of experiments were performed to determine the effects of miR-605 upregulation on NSCLC cell proliferation, apoptosis, migration and invasion in vitro and tumor growth in vivo. In addition, the downstream regulatory mechanisms of miR-605 action in NSCLC cells were explored. Decreased expression of miR-605 was frequently detected in NSCLC tissues and cell lines. Low expression of miR-605 was significantly correlated with the tumor size, TNM stage, and distane metastasis in NSCLC patients. Exogenous miR-605 expression inhibited proliferation, increased apoptosis, and inhibited metastasis of NSCLC cells in vitro. Additionally, miR-605 overexpression hindered the growth of NSCLC cells in vivo. Furthermore, Forkhead Box P1 (FOXP1) was identified as a direct target gene of miR-605 in NSCLC cells. Moreover, FOXP1 was highly expressed in NSCLC cells and showed an inverse correlation with miR-605 expression levels. Besides, silencing of FOXP1 simulated roles similar to miR-605 upregulation in NSCLC cells. FOXP1 reintroduction partially abolished the anticancer effects of miR-605 in NSCLC cells. Our results revealed that miR-605 inhibited the oncogenicity of NSCLC cells in vitro and in vivo by directly targeting FOXP1, suggesting the importance of the miR-605/FOXP1 pathway in the malignant development of NSCLC.