rheumatoid arthritis (ra) is a common systemic autoimmune disorder of unknown etiology, which threatens public health. The regulatory role of tripartite motif-containing 22 (TriM22) has been reported in multiple types of cancers and disease, but not in ra. The aim of the present study was therefore to elucidate the potential roles and underlying mechanisms of TRIM22 in fibroblast-like synoviocytes (FlSs) in ra. The Gene expression omnibus database was used to examine TRIM22 mRNA expression levels in synovial tissue samples of patients with RA and healthy controls. TriM22 and forkhead box c1 (FoXc1) mrna and protein expression levels in normal FLSs and RA-FLSs were assessed using reverse transcription-quantitative PCR (RT-qPCR) and western blotting, respectively. The Cell Counting Kit-8 assay was used to assess cell proliferation. cell apoptosis was analyzed using flow cytometry. The migratory and invasive abilities of ra-FlSs were assessed using Transwell assays.Western blotting was used to analyze the protein expression levels of apoptosis-related factors, MMP2, MMP9 and NF-κB signaling pathway-related proteins. inflammatory factors levels were assessed via ELISA and RT-qPCR. Furthermore, the JaSPar database, chromatin immunoprecipitation and the dual-luciferase reporter assays were used to determine the interaction between FoXc1 and the TriM22 promoter. The results of the present study demonstrated that TriM22 expression levels were significantly elevated in the synovial tissue samples of patients with RA and RA-FLSs. Moreover, FOXC1 was also significantly overexpressed in RA-FLSs. TRIM22 knockdown significantly reduced cell proliferation, migration, invasion and the inflammatory response, whereas cell apoptosis was significantly increased. Furthermore, the results demonstrated that FOXC1 may have positively mediated TRIM22 expression via binding to the TRIM22 promoter. Moreover, FOXC1 overexpression significantly reversed the outcome of TriM22 knockdown on the proliferation, apoptosis, migration, invasion and inflammation of RA-FLSs. FOXC1 overexpression also significantly reversed the inactivation of the nF-κB signaling pathway caused by TriM22 knockdown. in summary, the present study demonstrated that TriM22 was potentially activated via FOXC1, which contributed to the progression of RA via the NF-κB signaling pathway.

Objectives: This study aims to explore the mechanism by which long non-coding ribonucleic acids (lncRNA) X-inactive specific transcript (XIST) affects the progression of adjuvant-induced arthritis (AIA). Materials and methods: Freund's complete adjuvant was used to induce arthritis in rats. The polyarthritis, spleen and thymus indexes were calculated to evaluate AIA. Hematoxylin-eosin (H&E) staining was used to reveal the pathological changes in the synovium of AIA rats. Enzyme-linked immunosorbent assay (ELISA) was performed to detect the expression of tumor necrosis factor-alpha (TNF-α), interleukin (IL)-6 and IL-8 in the synovial fluid of AIA rats. The cell continuing kit (CCK)-8, flow cytometry, and Transwell assays were used to assess the proliferation, apoptosis, migration and invasion of transfected fibroblast-like synoviocytes (FLS) isolated from AIA rats (AIA-FLS). Dual-luciferase reporter assay was performed to verify the binding sites between XIST and miR-34b-5p or between YY1 mRNA and miR-34b-5p. Results: The XIST and YY1 were highly expressed, and miR-34a-5p was lowly expressed in the synovium of AIA rats and in AIA-FLS. Silencing of XIST impaired the function of AIA-FLS in vitro and inhibited the progression of AIA in vivo. The XIST promoted the expression of YY1 by competitively binding to miR-34a-5p. Inhibition of miR-34a-5p strengthened the function of AIA-FLS by upregulating XIST and YY1. Conclusion: The XIST controls the function of AIA-FLS and may promote the progression of rheumatoid arthritis via the miR-34a-5p/YY1 axis.