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.