期刊
ENVIRONMENTAL TOXICOLOGY
卷 36, 期 12, 页码 2484-2492出版社
WILEY
DOI: 10.1002/tox.23361
关键词
MINK1; miR-17-5p; rheumatoid arthritis; SNHG14
High expression of SNHG14 in rheumatoid arthritis is closely related to disease activity, promoting disease development through the miR-17-5p/MINK1 axis. Knockdown of SNHG14 significantly inhibits cell proliferation and inflammatory response.
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.
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