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.

Molecular Medicine Reports
|December 20, 2017
PubMed

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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