MicroRNA-133 suppresses cell viability and migration of rheumatoid arthritis fibroblast-like synoviocytes by down-regulation of MET, EGFR, and FSCN1 expression.
Shih-Yao ChenJeng-Long HsiehPo-Ting WuAi-Li ShiauChao-Liang WuPublished in: Molecular and cellular biochemistry (2022)
Aberrant proliferation and migration of fibroblast-like synoviocytes (FLS) are major characteristics of rheumatoid arthritis (RA). MicroRNA-133 (miR-133) is a tumor-suppressive miRNA that targets various genes responsive for cell proliferation and migration. The aim of this study was to examine the effect of miR-133 on RA FLS. A high throughput miRNA microarray was performed in synovium from mice with collagen-induced arthritis (CIA). Expression levels of miR-133 and the putative targets were determined in synovium and FLS from patients with RA and mice with CIA. Overexpression of miR-133 in RA FLS was performed by lentiviral vector-mediated transfer of precursor miRNA (pre-miR). The expression of miR-133a/b was decreased in the joint tissue and FLS of CIA mice, as determined by miRNA array and qRT-PCR. Down-regulation of miR-133a/b expression could also be observed in synovium and FLS from patients with RA. Overexpression of miR-133 reduced cell viability and migration of RA FLS, with decreased levels of FSCN1, EGFR, and MET. Our findings demonstrated the inhibitory effects of miR-133 on FLS viability and migration, and might contribute to the pharmacologic development of miR-133 therapeutics in patients with RA.
Keyphrases
- cell proliferation
- rheumatoid arthritis
- long non coding rna
- poor prognosis
- long noncoding rna
- disease activity
- high throughput
- small cell lung cancer
- ankylosing spondylitis
- interstitial lung disease
- tyrosine kinase
- stem cells
- type diabetes
- single cell
- adipose tissue
- binding protein
- endothelial cells
- high resolution
- bone marrow
- mesenchymal stem cells
- oxidative stress
- dna methylation
- small molecule
- mass spectrometry
- bioinformatics analysis