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Maternally expressed gene 3 (MEG3) in rheumatoid arthritis (RA) and its underlying mechanism were explored. Synovial tissues from 10 RA patients and 10 controls were collected to detect MEG3 expression in fibroblast-like synoviocytes (FLS). The relationship between MEG3 expression and TNF-α was analyzed. After MEG3 knockdown by lentivirus transfection, cell cycle, proliferation, apoptosis, invasion and secretion of inflammatory factors were detected. Furthermore, the effect of MEG3 on STAT3 and PI3K/AKT pathways was explored. MEG3 was downregulated in RA patients, and exogenous TNF-α treatment could decrease MEG3 expression. After transfection with lentivirus, downregulated MEG3 led to FLS proliferation and secretion of inflammatory cytokines, IL-6 and IL-8, improved the invasive ability and inhibited apoptosis. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) results revealed that downregulated MEG3 increased the expression levels of MMP2 and MMP9. Western blotting results showed that downregulated MEG3 activated STAT3 and PI3K/AKT pathways. Downregulated MEG3 was able to promote proliferation and invasion, and inhibit apoptosis of FLS via STAT3 pathway.

Downregulated MEG3 participates in rheumatoid arthritis via promoting proliferation of fibroblast‑like synoviocytes