ArticleBMC immunology2024
Upregulated miR-146b-3p predicted rheumatoid arthritis development and regulated TNF-α-induced excessive proliferation, motility, and inflammation in MH7A cells.
Article in BMC immunology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- METTL3-Mediated m6A Regulation of CircINTS4/miR-146b-3p Axis in Rheumatoid Arthritis.Inflammation · 2026Article
- Proceedings of cell-free noncoding RNA biomarker studies in liquid biopsy.Rheumatology and immunology research · 2025Article
- Role of Non-coding RNAs in Rheumatoid Arthritis and Supervision Mechanism of Chinese Medicine.Chinese journal of integrative medicine · 2025Review
- LncRNA CYP1B1-AS1 as a clinical biomarker exacerbates sepsis inflammatory response via targeting miR- 18a- 5p.BMC immunology · 2025Article
- [LINC00837/miR-671-5p/SERPINE2 functional axis promotes pathological processes of fibroblast-like synovial cells in rheumatoid arthritis].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2025Article
- METTL3-mediated methylation of RAC2 contributes to cell motility, oxidative stress and inflammation in TNF-α-stimulated rheumatoid arthritis fibroblast-like synovial cells.Journal of orthopaedic surgery and research · 2025Article
- HMGCR: a malignancy hub - frontiers in cancer diagnosis and therapy.Frontiers in oncology · 2025Review
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Authors and funding
4 authors.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundRheumatoid arthritis (RA) is a chronic immune system disease with a high disability rate threatening the living quality of patients. Identifying potential biomarkers for RA is of necessity to improve the prevention and management of RA.
objectivesThis study focused on miR-146b-3p evaluating its clinical significance and revealing the underlying regulatory mechanisms. MATERIALS AND
methodsA total of 107 RA patients were enrolled, and both serum and synovial tissues were collected. Another 78 osteoarthritis patients (OA, providing synovial tissues), and 72 healthy individuals (providing serum samples) were enrolled as the control group. The expression of miR-146b-3p was analyzed by PCR and analyzed with ROC and Pearson correlation analyses evaluating its significance in diagnosis and development prediction of RA patients. In vitro, MH7A cells were treated with TNF-α. The regulation of cell proliferation, motility, and inflammation by miR-146b-3p was assessed by CCK8, Transwell, and ELISA assays.
resultsSignificant upregulation of miR-146b-3p was observed in serum and synovial tissues of RA patients, which distinguished RA patients and were positively correlated with the erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), anti-cyclic citrullinated peptide antibodies (anti-CCP), and rheumatoid factor (RF) of RA patients. TNF-α promoted the proliferation and motility of MH7A cells and induced significant inflammation in cells. Silencing miR-146b-3p alleviated the effect of TNF-α and negatively regulated the expression of HMGCR. The knockdown of HMGCR reversed the protective effect of miR-146b-3p silencing on TNF-α-stimulated MH7A cells.
conclusionsIncreased miR-146b-3p served as a biomarker for the diagnosis and severity of RA. Silencing miR-146b-3p could suppress TNF-α-induced excessive proliferation, motility, and inflammation via regulating HMGCR in MH7A cells.
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