miR-766-3p promotes non-small cell lung cancer development through suppression of NR3C2.

Abstract

The incidence of non-small cell lung cancer (NSCLC) has exhibited an elevated trend yearly, seriously threatening human health. However, its molecular mechanism is still unknown. The objective of this experiment was to investigate the expression and prognostic value of miR-766-3p in the tissues of NSCLC patients, as well as to provide possible targets for the healing of NSCLC. In this study, miR-766-3p and nuclear receptor subfamily 3 group C member 2 (NR3C2) were detected in tissues of NSCLC patients using reverse transcription quantitative real-time polymerase chain reaction (RT-qPCR). Survival analysis was estimated with Kaplan-Meier and Cox proportional hazards model. In vitro experiments included Cell Counting Kit-8 (CCK-8) viability assay, flow cytometry for apoptosis, Transwell assay for migration and invasion, and luciferase reporter assay for target genes. miR-766-3p levels were clearly elevated in tumor tissues, and high miR-766-3p levels were considered to be a poor prognostic factor. NR3C2 was clearly down-regulated in the serum of NSCLC patients. miR-766-3p overexpression stimulated the proliferation and enhanced metastatic spread of lung cancer cells, whereas down-regulation of NR3C2 reversed the effect of miR-766-3p on cellular activity. miR-766-3p promotes NSCLC development by inhibiting NR3C2 levels and is a potential biomarker. Furthermore, high levels of miR-766-3p are likely to predict poor prognosis in NSCLC.