Abstract
It is reported that miR-129-5p plays an important role in various diseases, but its effect on rheumatoid arthritis (RA) and the potential mechanism remain to be clarified. In the present research, we aimed to investigate the effect of miR-129-5p on RA and the special molecular mechanism. First, the expression of miR-129-5p was analyzed in RA patients and RA Fibroblast-like synoviocytes (RA-FLSs) by RT-PCR assay. The cell viability, apoptotic rate and the relative expression of caspase-3 and caspase-8 were measured by CCK-8, Annexin-FITC/propidium iodide (PI) and ELISA, respectively. Luciferase reporter assay was performed to investigate the target of miR-129-5p. The results revealed that the expression of miR-129-5p was down-regulated in RA patients and RA-FLSs. In addition, miR-129-5p inhibited cell proliferation and induced apoptosis of RA-FLS. Furthermore, luciferase reporter assay demonstrated that insulin-like growth factor-1 receptor (IGF-1R) was the direct target of miR-129-5p, and IGF-1R promoted cell proliferation and inhibited apoptosis by activating Src/ERK/Egr-1 signaling. Furthermoremore, the Src/ERK/Egr-1 signaling pathway was suppressed by miR-129-5p. Collectively, the results of the present study suggested that miR-129-5p regulated cell proliferation and apoptosis via IGF-1R/Src/ERK/Egr-1 signaling pathway in RA.
Highlights
Rheumatoid arthritis (RA) is a joint disease caused by chronic inflammation, and the most important clinical feature is chronic arthritis, which will eventually lead to bone destruction, cartilage, bone damage and disability [1,2]
The results of the present study suggested that miR-129-5p inhibits cell proliferation and induces apoptosis of rheumatoid arthritis (RA)-FLS via Src/ERK/Egr-1 signaling by directly target insulin-like growth factor-1 receptor (IGF-1R) in RA
In order to determine the expression of miR-129-5p in RA patients and RA Fibroblast-like synoviocyte (RA-FLS), 15 tissues and serums with RA as well as 12 normal human control tissues and serums were analyzed by qRT-PCR
Summary
Rheumatoid arthritis (RA) is a joint disease caused by chronic inflammation, and the most important clinical feature is chronic arthritis, which will eventually lead to bone destruction, cartilage, bone damage and disability [1,2]. The main clinical treatment strategy of RA is drug therapy, including immunosuppressive drugs and biological agents. These therapies induce a general drug resistance that increases the risk of infectious diseases and cancer [4,5]. A large number of studies have shown that most miRNAs in various cancer cells are abnormally expressed. In recent years, increasing evidences have shown that miRNAs play important roles in the occurrence and development of RA by regulating cell viability, apoptosis, and invasion [9,10]. Previous studies have shown that miR-129-5p is an important tumor suppressor, and overexpression of miR-129-5p significantly reduces the proliferation, migration and invasion
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