ArticleJournal of orthopaedic surgery and research2025
METTL3-mediated methylation of RAC2 contributes to cell motility, oxidative stress and inflammation in TNF-α-stimulated rheumatoid arthritis fibroblast-like synovial cells.
Article in Journal of orthopaedic surgery and research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- The effect of mobilization with movement on pain, joint distance, effusion area, and inflammation in rheumatoid arthritis: a double-blind randomized controlled clinical trial.Journal of orthopaedic surgery and research · 2025Trial
- Clerodendrum japonicum Extract Suppresses the Pathogenicity of Rheumatoid Arthritis Fibroblast-Like Synoviocytes by Inhibiting METTL3-Mediated ICAM2 mRNA Methylation.Cell biochemistry and function · 2026Article
- Bioinformatics analysis reveals shared gene signatures and molecular mechanisms between periodontitis and rheumatoid arthritis in the context of aging.Acta odontologica Scandinavica · 2026Article
- The role and therapeutic prospects of intercellular communication and RNA mFrontiers in immunology · 2026Review
- Epitranscriptomic regulation by m6A in immunity and autoimmune disorders: emerging mechanisms and clinical perspectives.Frontiers in immunology · 2026Review
- The PANoptotic mosaic of rheumatoid arthritis: epitranscriptomic regulation, systemic relays, and precision death-mode editing.Frontiers in immunology · 2026Review
- Decoding Rho GTPase signalling networks in directed cell migration.Frontiers in cell and developmental biology · 2026Review
- RNA methylation in autoimmune rheumatic diseases: mechanisms and therapeutic potential.Frontiers in immunology · 2026Review
- Epigenetic modifier m⁶A methylation: insights into the pathogenesis and therapeutic potential of autoimmune diseases.Journal of translational medicine · 2025Review
- Pharmacological Inhibition of the PI3K/AKT/mTOR Pathway in Rheumatoid Arthritis Synoviocytes: A Systematic Review and Meta-Analysis (Preclinical).Pharmaceuticals (Basel, Switzerland) · 2025Review
- Methyltransferase-like 3-mediated RNA NFrontiers in immunology · 2025Review
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Authors and funding
7 authors.
Funding
Abstract
backgroundRheumatoid arthritis (RA) is a widely prevalent rheumatic condition causing joint inflammation and damage. RNA methylation plays an important role in RA. Herein, we intended to investigate the function of methyltransferase-like 3 (METTL3) and its N6-methyladenosine (m6A) methylation regulation for ras-related C3 botulinum toxin substrate 2 (RAC2) in RA.
methodsMH7A cells were treated with TNF-α to establish RA cell model. The expression analysis was performed by RT-qPCR and western blot. Cellular behaviors were examined by CCK-8 assay, flow cytometry, wound healing assay and transwell assay. Oxidative stress was assessed by detecting the associated indicators. Inflammatory cytokines were measured via enzyme-linked immunosorbent assay (ELISA). Interaction between METTL3 and RAC2 was analyzed via RNA immunoprecipitation (RIP) assay and MeRIP assay.
resultsRAC2 was highly expressed in RA tissues and TNF-α-stimulated MH7A cells. Knockdown of RAC2 enhanced apoptosis and reduced proliferation, migration, invasion after TNF-α treatment. RAC2 downregulation suppressed oxidative stress and inflammatory response in TNF-α-treated MH7A cells. METTL3 promoted RAC2 expression through m6A methylated modification, and METTL3/RAC2 could activate AKT pathway. RAC2 overexpression reversed the effects of METTL3 knockdown on cell proliferation, motility, oxidative stress and inflammation.
conclusionThe above results demonstrated that METTL3 facilitated the progression of RA via downregulating RAC2 in an m6A dependent mechanism in TNF-α-treated MH7A cells.
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