Oncogenic role of miR-183-5p in lung adenocarcinoma: A comprehensive study of qPCR, in vitro experiments and bioinformatic analysis

Despite the fact that previous studies have reported the aberrant expression of miR-183-5p in lung adenocarcinoma (LUAD), the oncogenic role of miR-183-5p in LUAD and its underlying mechanisms have remained elusive. Hence, we attempted to elucidate the clinicopathological significance of miR-183-5p expression in LUAD and identify the biological function of miR-183-5p in LUAD in this study. Meta-analysis of Gene Expression Omnibus (GEO) data, data mining of The Cancer Genome Atlas (TCGA) and real-time quantitative polymerase chain reaction (qPCR) were performed to evaluate the clinicopathological significance of miR-183-5p in LUAD. Then, the effect of miR-183-5p on cell growth in LUAD was assessed by in vitro experiments. Additionally, the target genes of miR-183-5p were identified via miRWalk v.2.0 and TCGA. Gene Ontology (GO) analysis, Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis and Disease Ontology (DO) analysis were further carried out for the target genes. The targetability between target genes in key KEGG pathways and miR-183-5p was validated by independent samples t-test, Pearson's correlation test and immunohistochemistry results from the Human Protein Atlas (HPA). According to the results, miR-183-5p was overexpressed in LUAD and exhibited significant diagnostic value. Moreover, miR-183 expression was associated with tumor progression in the TCGA data. In vitro experiments revealed the positive influence of miR-183-5p on cell viability and proliferation as well as the negative effect of miR-183-5p on caspase-3/7 activity in LUAD, which supports the finding that target genes of miR-183-5p are mainly enriched in gene pathways containing cell adhesion molecules (CAMs) and gene pathways important in cancer. Therefore, we conclude that miR-183-5p acts as an oncogene in LUAD and participates in the pathogenesis of LUAD via the interaction networks of its target genes.