MiR-137 decreases proliferation, migration and invasion in rheumatoid arthritis fibroblast-like synoviocytes

Abstract

MicroRNA-137 (miR-137) is involved in cell proliferation, migration, invasion and apoptosis in a variety of cells. However, the role of miR-137 in rheumatoid arthritis (RA) remains unclear. The present study aimed to identify the biological roles of miR-137 in RA. The expression of miR-137 in RA fibroblast-like synoviocytes (RA-FLS) and in normal control FLS was detected by reverse transcription-quantitative polymerase chain reaction (RT-qPCR). The effects of miR-137 on RA-FLS proliferation, migration and invasion were also determined using MTT, wound healing and Transwell invasion assays, respectively. The effects of miR-137 on inflammatory cytokine expression in RA-FLS were assessed by ELISA. Bioinformatics databases (TargetScan and miRanda), luciferase reporter assays, RT-qPCR and western blotting assays were conducted to identify potential target genes. miR-137 expression was decreased in RA-FLS compared with expression in normal control FLS. Overexpression of miR-137 resulted in a significant reduction in RA-FLS proliferation, migration and invasion, and decreased the expression of inflammatory cytokines of RA-FLS. In addition, bioinformatics analysis and luciferase reporter assays indicated that miR-137 may target the 3'-untranslated region of C-X-C motif chemokine ligand 12 (CXCL12), which was confirmed by RT-qPCR and western blot analyses. These results further demonstrated that miR-137may serve an inhibitory role in RA by targeting CXCL12 expression, and miR-137 may be a potential target for the treatment of RA.