Regulatory interactions between long noncoding RNA LINC00968 and miR‑9‑3p in non‑small cell lung cancer: A bioinformatic analysis based on miRNA microarray, GEO and TCGA.

Long non‑coding RNAs (lncRNAs) have been demonstrated to mediate carcinogenesis in various types of cancer. However, the regulatory role of lncRNA LINC00968 in lung adenocarcinoma remains unclear. The microRNA (miRNA) expression in LINC00968‑overexpressing human lung adenocarcinoma A549 cells was detected using miRNA microarray analysis. miR‑9‑3p was selected for further analysis, and its expression was verified in the Gene Expression Omnibus (GEO) database. In addition, the regulatory axis of LINC00968 was validated using The Cancer Genome Atlas (TCGA) database. Results of the GEO database indicated miR‑9‑3p expression in lung adenocarcinoma was significantly higher compared with normal tissues. Functional enrichment analyses of the target genes of miR‑9‑3p indicated protein binding and the AMP‑activated protein kinase pathway were the most enriched Gene Ontology and KEGG terms, respectively. Combining target genes with the correlated genes of LINC00968 and miR‑9‑3p, 120 objective genes were obtained, which were used to construct a protein‑protein interaction (PPI) network. Cyclin A2 (CCNA2) was identified to have a vital role in the PPI network. Significant correlations were detected between LINC00968, miR‑9‑3p and CCNA2 in lung adenocarcinoma. The LINC00968/miR‑9‑3p/CCNA2 regulatory axis provides a new foundation for further evaluating the regulatory mechanisms of LINC00968 in lung adenocarcinoma. [ABSTRACT FROM AUTHOR]