MiR-593-5p inhibited proliferation and migration of lung adenocarcinoma by targeting ICAM-1.

Abstract

The aim of this study was to investigate the role of microRNA-593-5p (miR-593-5p) in the development of lung adenocarcinoma (LA). The expression level of miR-593-5p in LA tissues and cell lines was detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Luciferase reporter gene assay and Western blot were performed to evaluate the interaction between miR-593-5p and intercellular cell adhesion molecule-1 (ICAM-1). Furthermore, the effects of the miR-593-5p/ICAM-1 axis on A549 cells were determined by MTS, colony formation assay, and transwell assay, respectively. MiR-593-5p was significantly downregulated in both clinical samples and cell lines. The bioinformatics analysis predicted that miR-593-5p could complementarily bind to the 3'-UTR of ICAM-1. Luciferase reporter gene assay confirmed that ICAM-1 was the direct target of miR-593-5p. Western blot results demonstrated that miR-593-5p could effectively reduce the protein expression of ICAM-1 in cells. In vitro experiments indicated that the proliferation and migration of A549 cells were significantly inhibited by miR-593-5p transfection. However, the overexpression of ICAM-1 could effectively reverse the inhibitory effects of miR-593-5p in vitro. These results indicated that the inhibitory effects of miR-593-5p on LA were achieved by regulating ICAM-1 expression. MiR-593-5p/ICAM-1 axis might be a potential therapeutic target for the diagnosis and treatment of LA.