Down-regulation of microRNA-142-3p inhibits the aggressive phenotypes of rheumatoid arthritis fibroblast-like synoviocytes through inhibiting nuclear factor-κB signaling

摘要: The present study aimed to investigate the regulatory roles of miR-142-3p on aggressive phenotypes rheumatoid arthritis (RA) human fibroblast-like synoviocytes (RA-HFLSs), and reveal potential mechanisms relating with nuclear factor-κB (NF-κB) signaling. expression was detected in RA synovial tissues RA-HFLSs by quantitative real-time PCR (qRT-PCR) Northern blot analysis. were transfected inhibitor and/or treated 10 µg/l tumor necrosis factor α (TNF-α). viability, colony formation, apoptosis, migration, invasion, levels interleukin (IL)-6, matrix metalloproteinase 3 (MMP-3) detected. mRNA expressions B-cell lymphoma-2 (Bcl-2), Bax, Bad, IL-6, MMP-3 qRT-PCR. Moreover, Bcl-2, IL-1 receptor-associated kinase 1 (IRAK1), Toll-like receptor 4 (TLR4), NF-κB p65, phosphorylated p65 (p-NF-κB p65) Western blot. interaction between IRAK1 identified dual luciferase reporter gene assay. MiR-142-3p up-regulated RA-HFLSs. TNF-α activated RA-HFLSs, including enhanced proliferation, inflammation, inhibited apoptosis. significantly decreased cell number clones, migration rate, invasive cells, contents IL-6 MMP-3, increased apoptosis rate Bax Bcl-2 TNF-α-treated reversed TNF-α-induced up-regulation IRAK1, TLR4, p-NF-κB Besides, a target miR-142-3p. down-regulation through inhibiting