miR‐7641: A Novel Diagnostic Biomarker for Rheumatoid Arthritis That Exerts Protective Effects by Targeting TNFSF10

ABSTRACT Rheumatoid arthritis (RA) is closely associated with genetic factors, but there is still a lack of ideal biomarkers for its early diagnosis and precise intervention. To investigate the diagnostic value and synovial cell function of miR‐7641 in RA, and its mechanistic link to TNFSF10 . A case‐control study was conducted with 152 RA patients and 152 matched asymptomatic first‐degree relatives. Serum miR‐7641 and TNFSF10 levels were quantified by qRT‐PCR. Diagnostic accuracy was assessed via logistic regression and ROC analysis. In MH7A cells, miR‐7641 mimic/inhibitor transfection was performed, followed by assessments of proliferation (CCK‐8), inflammatory cytokines (ELISA), and target interaction (dual‐luciferase assay). Rescue experiments involved co‐transfection of the miR‐7641 mimic and a TNFSF10 overexpression plasmid. Serum miR‐7641 was downregulated in RA patients and identified as an independent protective factor with high diagnostic accuracy (AUC = 0.902). In MH7A cells, miR‐7641 overexpression suppressed proliferation and reduced IL‐6, IL‐1β, and TNF‐α secretion. TNFSF10 was confirmed as a direct target, with its expression negatively correlating with miR‐7641 in serum samples. Importantly, TNFSF10 overexpression rescued the inhibitory effects of miR‐7641 on proliferation and cytokine production. This study identifies serum miR‐7641 as a potential diagnostic biomarker for RA. In an immortalized synovial cell model, miR‐7641 exerts protective effects by targeting TNFSF10 to inhibit proliferation and inflammation. Future studies in primary cells and in vivo models are required to validate these findings and explore downstream signalling mechanisms.