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Lung cancer is the most common type of cancer worldwide, the most prevalent form of which is non-small cell lung cancer (NSCLC). MicroRNAs (miRs) are involved in the progression of NSCLC; however, the specific function of miR-140-5p in NSCLC remains unclear. The present study demonstrated that miR-140-5p was downregulated in the tumor tissues of patients with NSCLC, and it was associated with a poor prognosis. Furthermore, miR-140-5p significantly suppressed cell migration and invasion of the NSCLC cell line A549. In addition, the direct regulatory effect of miR-140-5p on vascular endothelial growth factor-A (VEGFA) was predicted by TargetScan and verified using a luciferase reporter gene assay. The present study also hypothesized that miR-140-5p may inhibit the expression of phosphorylated-protein kinase B by targeting VEGFA. In conclusion, miR-140-5p may be a potential target for the development of anti-neoplastic therapies in lung cancer. [ABSTRACT FROM AUTHOR]

Non-small-cell lung cancer (NSCLC) accounts for 80% of lung cancer cases, and is the leading cause of cancer-associated mortality worldwide. The present study aimed to investigate the roles of microRNA (miR)-654-3p in NSCLC. The expression levels of miR-654-3p and its target ras protein activator like 2 (RASAL2) mRNA were determined by reverse transcription-quantitative polymerase chain reaction; protein expression was analyzed by western blotting. Plasmids expressing miR-654-3p mimics were constructed and transfected into A549 cells. In addition, the viability and apoptotic rate of cells were analyzed by an MTT assay and flow cytometry, respectively. A luciferase reporter assay was performed to verify whether RASAL2 is a target of miR-654-3p. Downregulated miR-654-3p and upregulated RASAL2 expression were observed in tumor tissues and cells. Cell viability was suppressed and the apoptotic rate was increased in the miR-654-3p mimics-transfected cells compared with the control. Luciferase activity was decreased in the RASAL2-3′ untranslated region-wild type group treated with miR-654-3p mimics. Furthermore, the present study revealed that overexpression of miR-654-3p could suppress the viability and induce the apoptosis of cells by targeting RASAL2 in NSCLC. The present findings may contribute to developments in the treatment of NSCLC. [ABSTRACT FROM AUTHOR]