Effects of LINC00607-miR-103a-3p/miR-16-5p pathway on proliferation, apoptosis, and inflammation of fibroblast-like synoviocytes in rheumatoid arthritis

Abstract Objectives Rheumatoid arthritis (RA) is an autoimmune disease characterized by joint lesions caused by inflammation of the synovial membrane. This study investigates the potential mechanisms underlying RA pathogenesis. Methods The serum samples were collected from 66 healthy volunteers and 66 patients with RA for clinical expression analysis. RA-fibroblast-like synoviocytes (RA-FLS) were treated with 20 ng/mL TNF-α to construct an RA cell model. The method of 5-bromo-2′-deoxyuridine (BrdU) insertion was used to evaluate cell proliferation capacity. Cell apoptosis was determined by double staining with Annexin V-FITC/propidium iodide (PI). The inflammatory response was evaluated by measuring IL-6, IL-12, and IFN-γ levels. The dual luciferase reporter assay and the overexpressing plasmid transfection experiment were used to the targeted regulation verification of LINC00607 on miR-103a-3p and miR-16-5p. The effect of LINC00607-miR-103a-3p/miR-16-5p pathway in RA was evaluated by co-transfecting miR-103a-3p/miR-16-5p mimic and LINC00607 plasmid. Results LINC00607 was down-regulated in RA patients, whose overexpression reversed the abnormal proliferation, anti-apoptosis, and inflammation response in TNF-α-treated RA-FLS. The overexpression of LINC00607 decreased the cellular levels of miR-103a-3p and miR-16-5p. Transfecting miR-103a-3p or miR-16-5p mimic intensified the TNF-α-induced RA phenotypes in RA-FLS, which was rescued by the co-transfection of LINC00607 plasmid. Conclusions LINC00607 restrained the growth and inflammation of RA-FLS and accelerated apoptosis by regulating miR-103a-3p and miR-16-5p negatively, which may suppress RA development.