miR-296-3p targets APEX1 to suppress cell migration and invasion of non-small-cell lung cancer.

Non-small-cell lung cancer (NSCLC) is the most common cause of cancer-associated mortality worldwide. MicroRNAs (miRs) are a class of small non-coding RNAs that are commonly dysregulated in human cancer. The aim of the current study was to evaluate the effect of miR-296-3p on the cell migration and invasion of NSCLC. Pairs of tumor tissues and para-cancerous tissues (n=50) were collected from patients with NSCLC, and the expression of miR-296-3p was analyzed by reverse transcription-quantitative polymerase chain reaction (RT-qPCR). Additionally, tumor cell viability, migration and invasion were examined in vitro using Cell Counting Kit-8, wound healing and Matrigel assays, respectively. Furthermore, potential targets of miR-296-3p were screened for using TargetScan and validated using a dual-luciferase reporter assay. The expression levels of phosphoinositide-3-kinase (PI3K), AKT serine/threonine kinase (AKT), mammalian target of rapamycin (mTOR), matrix metallopeptidase 2 (MMP2) and SRY-box 4 (SOX4) were detected by RT-qPCR and western blot analysis. The data indicated that miR-296-3p was downregulated in tumor tissues compared with adjacent normal tissues. Overexpression of miR-296-3p inhibited NSCLC cell viability, migration and invasion in vitro. Furthermore, apurinic/apyrimidinic endodeoxyribonuclease 1 (APEX1) was identified as a direct target of miR-296-3p. APEX1 expression was upregulated in tumor tissues compared with para-cancerous tissues, and the mRNA and protein expression levels of APEX1 were decreased following transfection of NSCLC cells with miR-296-3p mimics compared with control cells. Additional investigations revealed that miR-296-3p was involved in regulating the PI3K/AKT/mTOR signaling pathway, and miR-296-3p mimics decreased the mRNA and protein expression levels of MMP2 and SOX4. In summary, the findings demonstrated that miR-296-3p may function as a tumor suppressor, and inhibits the migration and invasion of NSCLC cells by targeting APEX1. miR-296-3p is therefore a potential therapeutic molecular modulator of NSCLC.