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It has been demonstrated that the deregulation of microRNAs (miRNAs) affects the development of rheumatoid arthritis (RA). The primary objective of the current study was to determine the role of miR-143-3p in the progression of RA. The expression of miR-143-3p in synovium taken from patients with RA was assessed by reverse transcription-quantitative polymerase chain reaction. The expression of miR-143-3p was higher in synovium tissues of RA than that of osteoarthritis (OA). The decreased expression of miR-143-3p suppressed cell proliferation and promoted apoptosis in vitro . In addition, inhibition of miR-143-3p decreased levels of inflammatory cytokines, as determined by an enzyme-linked immunosorbent assay. IGF1R and IGFBP5 were found to be the target genes of miR-143-3p, and it was demonstrated that miR-143-3p regulated the proliferation and apoptosis of MH7A cells by targeting IGF1R and IGFBP5. Furthermore, TNF-α treatment stimulated the Ras/p38 mitogen activated protein kinase (MAPK) signaling pathway, whereas miR-143-3p inhibition suppressed it. The results of the current study indicate that miR-143-3p may regulate cell proliferation and apoptosis by targeting IGF1R and IGFBP5 expression and regulating the Ras/p38 MAPK signaling pathways. Therefore, miR-143-3p may be a novel therapeutic target in RA.

experimental and therapeutic medicine

miR-143-3p regulates cell proliferation and apoptosis by targeting IGF1R and IGFBP5 and regulating the Ras/p38 MAPK signaling pathway in rheumatoid arthritis