Abstract
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.