LncRNA SNHG14 contributes to proinflammatory cytokine production in rheumatoid arthritis via the regulation of the miR-17-5p/MINK1-JNK pathway.

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Tytuł:: LncRNA SNHG14 contributes to proinflammatory cytokine production in rheumatoid arthritis via the regulation of the miR-17-5p/MINK1-JNK pathway.
Autorzy:: Zhang J; Department of Rheumatism and Immunology, The Second Affiliated Hospital of Harbin Medical University, Harbin, China.
Lei H; Department of Rheumatism and Immunology, The Second Affiliated Hospital of Harbin Medical University, Harbin, China.
Li X; Department of Rheumatism and Immunology, The Second Affiliated Hospital of Harbin Medical University, Harbin, China.
Źródło:: Environmental toxicology [Environ Toxicol] 2021 Dec; Vol. 36 (12), pp. 2484-2492. Date of Electronic Publication: 2021 Sep 16.
Typ publikacji:: Journal Article
Język:: English
Imprint Name(s):: Original Publication: New York, NY : John Wiley & Sons, c1999-
MeSH Terms:: Arthritis, Rheumatoid*/genetics
MicroRNAs*/genetics
MicroRNAs*/metabolism
RNA, Long Noncoding*/genetics
RNA, Long Noncoding*/metabolism
Protein Serine-Threonine Kinases/*metabolism
Cell Proliferation ; Cytokines/genetics ; Humans ; MAP Kinase Signaling System
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Contributed Indexing:: Keywords: MINK1; SNHG14; miR-17-5p; rheumatoid arthritis
Substance Nomenclature:: 0 (Cytokines)
0 (MIRN17 microRNA, human)
0 (MicroRNAs)
0 (RNA, Long Noncoding)
EC 2.7.11.1 (MINK1 protein, human)
EC 2.7.11.1 (Protein Serine-Threonine Kinases)
Entry Date(s):: Date Created: 20210916 Date Completed: 20211104 Latest Revision: 20220531
Update Code:: 20240105
DOI:: 10.1002/tox.23361
PMID:: 34529319
: Czasopismo naukowe

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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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