Rheumatoid arthritis (RA) is a widespread autoimmune disorder of the joints. Long noncoding RNAs (lncRNAs) have been reported to participate in the pathogenesis of RA by serving as competitive endogenous RNAs. LncRNA small nucleolar RNA host gene 14 (SNHG14) is involved in the development of various diseases. Here, we found that high expression of SNHG14 in RA was closely related to the disease activity. Functional assays indicated that SNHG14 knockdown obviously hampered phorbol myristate acetate-activated THP-1 (pTHP-1) cell proliferation and proinflammatory cytokines production. In mechanism, SNHG14 served as a sponge of microRNA-17-5p (miR-17-5p), and misshapen like kinase 1 (MINK1) was a target of miR-17-5p. SNHG14 depletion-induced inhibitory effects on cell proliferation and inflammatory response were reversed by MINK1 overexpression in macrophages. Moreover, SNHG14 promoted the jun N-terminal kinase (JNK) signaling via the miR-17-5p/MINK1 axis. Overall, SNHG14 boosted the process of RA by MINK1 activating the JNK pathway.

中文翻译：

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LncRNA SNHG14 通过调节 miR-17-5p/MINK1-JNK 通路促进类风湿性关节炎中促炎细胞因子的产生

类风湿性关节炎（RA）是一种广泛存在的关节自身免疫性疾病。据报道，长链非编码 RNA (lncRNA) 通过作为竞争性内源性 RNA 参与 RA 的发病机制。LncRNA小核仁RNA宿主基因14（SNHG14）参与多种疾病的发展。在这里，我们发现 RA 中 SNHG14 的高表达与疾病活动密切相关。功能测定表明，SNHG14 敲低明显阻碍了醋酸佛波醇肉豆蔻酸酯激活的 THP-1 (pTHP-1) 细胞增殖和促炎细胞因子的产生。在机制上，SNHG14 充当 microRNA-17-5p (miR-17-5p) 的海绵，畸形激酶 1 (MINK1) 是 miR-17-5p 的靶标。SNHG14 耗竭诱导的对细胞增殖和炎症反应的抑制作用被巨噬细胞中的 MINK1 过表达逆转。此外，SNHG14 通过 miR-17-5p/MINK1 轴促进 jun N 末端激酶 (JNK) 信号传导。总体而言，SNHG14 通过 MINK1 激活 JNK 通路促进了 RA 的进程。