MiR-124-3p Suppresses Prostatic Carcinoma by Targeting PTGS2 Through the AKT/NF-κB Pathway

• DOI: 10.1007/s12033-021-00326-7
• Publication Date: 2021-04-25T06:49:58Z
• Authors: Zhilei Zhang
• Keywords: Male; 0301 basic medicine; 0303 health sciences; Cell Survival; NF-kappa B; Prostatic Neoplasms; 3. Good health; Gene Expression Regulation, Neoplastic; MicroRNAs; 03 medical and health sciences; Cell Movement; Cyclooxygenase 2; Cell Line, Tumor; PC-3 Cells; Humans; Proto-Oncogene Proteins c-akt; Cell Proliferation; Signal Transduction

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.