LncRNA NEAT1 exacerbates non-small cell lung cancer by upregulating EIF4G2 via miR-582-5p sponging

Abstract

In this study, we aimed to elucidate the role of long non-coding RNA nuclear enriched abundant transcript 1 (lncRNA NEAT1) in non-small cell lung cancer (NSCLC). Quantitative real-time polymerase chain reaction (qRT-PCR) was employed to detect the abundance of NEAT1, microRNA-582-5p (miR-582-5p) and eukaryotic translation initiation factor 4 gamma 2 (EIF4G2). Proliferation, apoptosis, metastasis and glycolytic metabolism were determined by 3-(4,5-dimethylthiazol- 2-yl)-2,5-diphenyltetrazolium bromide (MTT) flow cytometry, transwell assays and fluorescence-based glucose and lactate assay kits. The targets of NEAT1 and miR-582-5p were predicted by the starBase website, and dual-luciferase reporter and RNA immunoprecipitation (RIP) assays were performed to verify these predictions. Western blot analysis was conducted to detect the protein expression of EIF4G2. A xenograft tumor model was built to clarify the role of NEAT1 in vivo. Results showed that NEAT1 interference inhibited proliferation, metastasis and glycolysis, and facilitated the apoptosis of NSCLC cells. MiR-582-5p was a functional target of NEAT1, and the biological influence of NEAT1 intervention on NSCLC cells was alleviated by transfection with anti-miR-582-5p. MiR-582-5p could bind to EIF4G2 messenger RNA (mRNA); it exerted its antitumor role in NSCLC cells by inhibiting EIF4G2. EIF4G2 was regulated by NEAT1/miR-582- 5p signaling. NEAT1 accelerated NSCLC tumor growth via the miR-582-5p/EIF4G2 axis in vivo. In conclusion, NEAT1 affected NSCLC by elevating their malignant potential via the miR-582-5p/EIF4G2 axis.

Keywords

• neat1
• mir-582-5p
• eif4g2
• metastasis
• glycolysis