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Updated: Feb 16, 2026

An Adoptive Transfer Model of Rheumatoid Arthritis in Mice
Published on: June 6, 2025
miR‑137 decreases proliferation, migration and invasion in rheumatoid arthritis fibroblast‑like synoviocytes
Juan Du1, Fangze Zhang2, Jialong Guo1
1Department of Rheumatology and Immunology, China‑Japan Union Hospital of Jilin University, Changchun, Jilin 130033, P.R. China.
Abstract:
MicroRNA-137 (miR-137) is involved in cell proliferation, migration, invasion and apoptosis in a variety of cells. However, the role of miR‑137 in rheumatoid arthritis (RA) remains unclear. The present study aimed to identify the biological roles of miR‑137 in RA. The expression of miR‑137 in RA fibroblast‑like synoviocytes (RA‑FLS) and in normal control FLS was detected by reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR). The effects of miR‑137 on RA‑FLS proliferation, migration and invasion were also determined using MTT, wound healing and Transwell invasion assays, respectively. The effects of miR‑137 on inflammatory cytokine expression in RA‑FLS were assessed by ELISA. Bioinformatics databases (TargetScan and miRanda), luciferase reporter assays, RT‑qPCR and western blotting assays were conducted to identify potential target genes. miR‑137 expression was decreased in RA‑FLS compared with expression in normal control FLS. Overexpression of miR‑137 resulted in a significant reduction in RA‑FLS proliferation, migration and invasion, and decreased the expression of inflammatory cytokines of RA‑FLS. In addition, bioinformatics analysis and luciferase reporter assays indicated that miR‑137 may target the 3'‑untranslated region of C‑X‑C motif chemokine ligand 12 (CXCL12), which was confirmed by RT‑qPCR and western blot analyses. These results further demonstrated that miR‑137may serve an inhibitory role in RA by targeting CXCL12 expression, and miR‑137 may be a potential target for the treatment of RA.
Insights
MicroRNA-137 (miR-137) is downregulated in rheumatoid arthritis (RA) fibroblast-like synoviocytes. Increasing miR-137 inhibits RA cell proliferation, migration, and invasion by targeting CXCL12, suggesting miR-137 as a potential RA therapeutic target.
Area of Science:
- Immunology
- Molecular Biology
- Genetics
Background:
- MicroRNA-137 (miR-137) regulates crucial cellular processes like proliferation and apoptosis.
- The specific role of miR-137 in rheumatoid arthritis (RA) pathogenesis is not well-defined.
Purpose of the Study:
- To elucidate the biological functions of miR-137 in RA.
- To investigate the potential of miR-137 as a therapeutic target for RA.
Main Methods:
- Quantitative reverse transcription PCR (RT-qPCR) to measure miR-137 expression.
- MTT, wound healing, and Transwell assays to assess RA fibroblast-like synoviocyte (RA-FLS) proliferation, migration, and invasion.
- ELISA, bioinformatics, luciferase reporter assays, RT-qPCR, and Western blotting to identify and validate miR-137 targets.
Main Results:
- miR-137 expression was significantly decreased in RA-FLS compared to normal FLS.
- Overexpression of miR-137 suppressed RA-FLS proliferation, migration, and invasion.
- miR-137 was identified as a direct targeting regulator of C-X-C motif chemokine ligand 12 (CXCL12) expression in RA-FLS.
Conclusions:
- miR-137 exhibits an inhibitory role in RA by targeting CXCL12.
- miR-137 represents a promising therapeutic candidate for managing rheumatoid arthritis.
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