miR-410-3p regulates proliferation and apoptosis of fibroblast-like synoviocytes by targeting YY1 in rheumatoid arthritis

• Published in: Biomedicine & pharmacotherapy 2019-11, Vol.119, p.109426-109426, Article 109426
• Main Authors: Wang, YueJiao, Jiao, Ting, Fu, WenYi, Zhao, Shuai, Yang, LiLi, Xu, NeiLi, Zhang, Ning
• Format: Article
• Language: English
• Subjects: Apoptosis; Apoptosis - genetics; Arthritis, Rheumatoid - genetics; Arthritis, Rheumatoid - pathology; Base Sequence; Cell Cycle - genetics; Cell Line; Cell Proliferation - genetics; Fibroblasts - metabolism; Fibroblasts - pathology; Humans; microRNAs; MicroRNAs - genetics; MicroRNAs - metabolism; Proliferation; Rheumatoid arthritis; Synoviocytes - metabolism; Synoviocytes - pathology; YY1 Transcription Factor - metabolism
• ISSN: 0753-3322; 1950-6007
• DOI: 10.1016/j.biopha.2019.109426

•Effect of miR-410-3p on RA FLS proliferation, apoptosis, & cell cycle was studied.•miR-410-3p levels were reduced in synovium and FLSs of patients with RA.•Up-regulated miR-410-3p inhibited proliferation and induced apoptosis.•Yin Yang 1 transcription factor was verified as a direct target gene of miR-410-3p.•Our findings might provide a potential therapeutic target for RA. In our previous study, miR-410-3p had been confirmed to regulate inflammatory cytokine release in rheumatoid arthritis fibroblast-like synoviocytes (RA FLSs). However, other biological functions of miR-410-3p in RA FLSs still remain unexplored. In the present study, we focused on the effect of miR-410-3p on proliferation, apoptosis, and cell cycle of RA FLSs, and explored the potential underlying mechanism. miR-410-3p mRNA levels in the synovium and FLSs of patients with RA and of healthy controls were quantitated by RT-qPCR. The levels of miR-410-3p were reduced in both synovium and FLSs from patients with RA. Next, we focused on the roles of miR-410-3p in cell viability, apoptosis, and cell cycle, by transfecting miR-410-3p mimics and inhibitor into RA FLSs, and conducting CCK-8 assay, EdU staining and flow cytometry. Results showed that miR-410-3p up-regulation suppressed proliferation, promoted apoptosis and G1-S phase transition while miR-410-3p down-regulation had opposite effects. YY1 was verified as a direct target gene of miR-410-3p through the luciferase reporter system; YY1 up-regulation was able to rescue the effects of miR-410-3p in RA FLSs. Taken together, our current findings might provide a potential therapeutic target for RA.