MicroRNA‑671‑5p inhibits cell proliferation, migration and invasion in non‑small cell lung cancer by targeting MFAP3L

MicroRNA (miR)‑671‑5p serves as a tumor suppressor in several types of cancer, including gastric and breast cancer. However, the function of miR‑671‑5p in non‑small cell lung cancer (NSCLC) has not been described in detail. The present study aimed to investigate the role of miR‑671‑5p in NSCLC. The expression levels of miR‑671‑5p were determined in NSCLC tissue samples and cell lines using reverse transcription‑quantitative PCR. Prediction of miR‑671‑5p targets was performed using the TargetScan database and verified by luciferase reporter assay and western blot analysis. Functional experiments, including Cell Counting Kit‑8, wound healing and Transwell assays, were performed in NSCLC cells. The results of the present study demonstrated that lower expression levels of miR‑671‑5p were observed in NSCLC tissues and cell lines compared with those in the corresponding controls. Low miR‑671‑5p levels were significantly associated with an advanced Tumor‑Node‑Metastasis stage and lymph node metastasis in patients with NSCLC. Microfibril‑associated protein 3‑like (MFAP3L) was confirmed to be a direct target of miR‑671‑5p. The proliferative, migratory and invasive abilities of NSCLC cells were suppressed following transfection with miR‑671‑5p mimics and promoted by the miR‑671‑5p inhibitor compared with those in the respective control groups. In addition, the effects of miR‑671‑5p on cell proliferation, migration and invasion, as well as the expression levels of proliferating cell nuclear antigen, E‑cadherin, N‑cadherin and vimentin were reversed by MFAP3L overexpression. In conclusion, targeting the miR‑671‑5p/MFAP3L signaling pathway may be a promising therapeutic strategy for NSCLC treatment.