MiRNA-6089 inhibits rheumatoid arthritis fibroblast-like synoviocytes proliferation and induces apoptosis by targeting CCR4

Abstract

Several studies have suggested that fibroblast-like synoviocytes (FLSs) and miRNAs are implicated in the pathogenesis of rheumatoid arthritis (RA). This study was aimed to evaluate the function of miR-6089 in the regulation of RA-FLSs. The levels of miR-6089 were detected to be significantly lower in the synovial tissues and FLSs of RA than in the healthy synovial tissues and FLSs. The miR-6089 up-regulation in RA-FLSs significantly inhibited the proliferation and promoted cell apoptosis accompany with an increase protein expression of cleaved-Caspase-3, -8 and -9. Furthermore, CCR4 was determined to target miR-6089 directly, and its expression was significantly increased in the synovial tissues of RA than in the healthy synovial tissues. The overexpression of CCR4 reversed the effect of miR-6089 on proliferation and apoptosis in RA-FLSs effectively. In conclusion, our study suggests that the miR-6089 may be a potential target for prevention and treatment of RA.

Keywords:

• MiRNA-6089
• rheumatoid arthritis
• fibroblast-like synoviocytes
• CCR4

Author contributions

S.L. wrote the manuscript and operated the experiments; Z.Z., S.W., Y.L., and M.Y. operated molecular experiments; P.C. and M.W. analysed the data; S.L. and M.W. designed the experiments and edited the manuscript. S.L. and C.L. revised the manuscript.

Disclosure statement

No potential conflict of interest has been reported by the author(s).

Date availability statement

All the required data are present in the article.

Additional information

Funding

This study was supported by Wenzhou Science and Technology Bureau Project [Y20160301 and 2017Y0539].