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