MicroRNA‑103 modulates tumor progression by targeting KLF7 in non‑small cell lung cancer.

Numerous studies have identified that microRNAs (miRs) play a crucial role in the tumorigenesis of non‑small cell lung cancer (NSCLC). However, to the best of our knowledge, the physiological function of miR‑103 in NSCLC is not fully understood. Experiments in the present study revealed that miR‑103 expression was increased in NSCLC cell lines. In addition, a series of methods, including MTT, colony formation, 5‑ethynyl‑2'‑deoxyuridine, Transwell, wound healing, flow cytometric, reverse transcription‑quantitative PCR and western blot assays, were performed, which revealed that overexpression of miR‑103 enhanced cell growth, migration, invasion and epithelial‑mesenchymal transition (EMT), and suppressed apoptosis of A549 and H1299 cells. Additionally, a dual‑luciferase reporter assay indicated that miR‑103 directly targets the 3'‑untranslated region of Kruppel‑like factor 7 (KLF7), and KLF7 expression was negatively regulated by miR‑103 expression. Furthermore, the present findings demonstrated that miR‑103 promoted EMT via regulating the Wnt/β‑catenin signaling pathway in NSCLC. Collectively, the current results demonstrated that miR‑103 serves a tumorigenesis role in NSCLC development by targeting KLF7, at least partly via the Wnt/β‑catenin signaling pathway. Consequently, these findings indicated that miR‑103/KLF7/Wnt/β‑catenin may provide a novel insight into underlying biomarkers for improving the diagnosis and treatment of NSCLC.