Overexpressed inflammatory cytokines are the main factors causing rheumatoid arthritis (RA) tissue damage and pathological deterioration, and lncRNAs has found to beinvolved in some autoinflammatory diseases.
We designed this study to investigate the effect of lncRNA linc00152 on rheumatoid arthritis inflammation and explore its molecular mechanism.
We found that linc00152 was not only up-regulated in rheumatoid arthritis fibroblast-like synoviocytes (RAFLS), but also stimulated by TNF-α/IL-1β in adose- and time-dependent manner in RAFLS and this expression depends on the NF-κB signaling pathway. Conversely, linc00152 promoted TNF-α/IL-1β expression in RAFLS induced by TNF-α/IL-1β. In addition, we found that linc00152 promoted TAK1 expression by targeting inhibition of miR-103a and activated TAK1-mediated NF-κB pathway. NF-kB indirectly promotes linc00152 expression by promoting the transcription activity of YY1, and YY1 directly promotes linc00152 expression by binding the promoter of linc00152.
Our data suggested that the linc00152/NF-κB feedback loop promotes RAFLS inflammation via regulating miR-103a/TAK1 axis and YY1 expression. Thus, linc00152 acts as a switch to control this regulatory circuit and may serve as a diagnostic and therapeutic target for RA treatment.