miR-202 functions as a tumor suppressor in non-small cell lung cancer by targeting STAT3.

MicroRNAs (miRNAs) are a group of non-protein‑coding, short single-stranded RNAs, which are considered as promising molecular markers and therapeutic targets in several cancers. The present study explored the expression patterns and functional roles of miR‑202 in non‑small cell lung cancer (NSCLC). The expression levels of miR‑202 were determined in NSCLC tissues and cell lines using reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR). The functional impact of miR‑202 overexpression on NSCLC cell viability, migration and invasion were evaluated using Cell Counting Kit‑8 reagent and Transwell migration and invasion assays, respectively. The molecular mechanism underlying the tumor suppressive roles of miR‑202 on NSCLC was examined using bioinformatics analysis, luciferase reporter assay, RT‑qPCR and western blot analysis. In addition, signal transducer and activator of transcription (STAT) 3 was overexpressed to investigate the impact on miR‑202‑mediated tumor suppression in NSCLC. The results indicated that miR‑202 was downregulated in NSCLC tissues and cell lines, and was associated with tumor node metastasis stage and lymph node metastasis. Exogenous miR‑202 expression reduced NSCLC cell viability, migration and invasion. Furthermore, STAT3 was identified as a direct target gene of miR‑202 in NSCLC. STAT3 overexpression improved miR‑202‑impaired cell viability, migration and invasion. In conclusion, the present study revealed novel anticancer effects induced by miR‑202 upregulation in NSCLC, and indicated that STAT3 may be a molecular target of miR‑202.