MiR-124-3p通过靶向PTGS2调控AKT/NF-κB通路抑制前列腺癌的机制研究

Abstract

MiR-124-3p had shown its tumor-regulatory properties in different cancers, but its potential roles in prostatic carcinoma had not been clearly understood. This study aimed to explore the roles of miR-124-3p in the regulation of prostatic carcinoma. The expression levels of PTGS2 and miR-124-3p were detected in prostatic carcinoma tissues and cultivated cell lines with qRT-PCR, immunohistochemistry and western blot, respectively. The interaction between miR-124-3p and PTGS2 was verified by the dual-luciferase reporter assay. Western blot, MTT, colony formation and flow cytometry assays were performed to evaluate the mediatory roles of miR-124-3p in prostatic carcinoma cells and the involvement of molecular pathways. Both prostatic carcinoma tissues and cells expressed a lower level of miR-124-3p and a higher level of PTGS2. PTGS2 was confirmed to be a target of miR-124-3p. MiR-124-3p suppressed cell viability, proliferation, migration, invasion and enhanced apoptosis of prostatic carcinoma cells by directly sponging PTGS2 to inhibit the AKT/NF-κB pathway. These findings provided information that miR-124-3p exerted anti-tumor effects in prostatic carcinoma by targeting PTGS2 to inactivate the AKT/NF-κB pathway. MiR-124-3p might have the potential to become an emerging therapeutic target for the treatment of prostatic carcinoma.