Receptor interacting serine/threonine kinase 2 promotes rheumatoid arthritis progression and partially regulates nuclear factor kappa B pathway.

Objective: Rheumatoid arthritis (RA) is a disabling systemic autoimmune disease worldwide; however, its molecular pathway remains largely unknown. Thus, this study aimed to explore the effects of receptor-interacting serine/threonine kinase 2 (RIPK2) on RA progression and its underlying mechanism.

Material and methods: RIPK2 expression was analyzed using real-time quantitative polymerase chain reaction, immunohistochemical staining, and Western blot (WB) analysis in RA synovial tissues or cells. Cell viability or proliferation was determined using the cell counting kit-8 and 5-ethynyl-2'-deoxyuridine. Cell metastasis was analyzed using the transwell assay and wound healing assay. Flow cytometry was adopted to measure cell apoptosis. The level of inflammation-related factors was measured using the enzyme-linked immunosorbent assay. WB analysis was used to determine the expression level of nuclear factor kappa B (NF-κB) pathway-related genes.

Results: RIPK2 was highly expressed in RA synovial tissues and cells. Transfection with RIPK2 short hairpin RNA plasmids reduced the gene expression level of RIPK2 in RA fibroblast-like synoviocytes (FLS) cells. Notably, RIPK2 silencing hindered the proliferation, invasion, and migration of tumor cells as well as accelerated the apoptosis of RA-FLS cells. Furthermore, RIPK2 silencing suppressed the RA-FLS cell inflammatory response and NF-κB pathway.

Conclusion: RIPK2 silencing could retrain the malignant behavior and inflammatory response of RA-FLSs and partially modulate the NF-κB pathway.