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MicroRNA-663 activates the canonical Wnt signaling through the adenomatous polyposis coli suppression.
- Source :
-
Immunology letters [Immunol Lett] 2015 Jul; Vol. 166 (1), pp. 45-54. Date of Electronic Publication: 2015 May 28. - Publication Year :
- 2015
-
Abstract
- Rheumatoid arthritis (RA) is a symmetrical polyarticular autoimmune disease of unknown etiology. In this present study, we observed that the adenomatous polyposis coli (APC) expression is down-regulated and the expression of microRNA (miR)-663 increased significantly in synovium from RA patients compared with control. Target gene prediction for miR-663 revealed that the mRNA of APC gene, which is a member of the canonical Wnt signaling pathway, has a miR-663 binding site in its 3'-untranslated region (3'UTR). The result showed that increased miR-663 suppressed the APC expression significantly, and this down-regulation of APC expression triggered the activation of canonical Wnt signaling through accumulation of β-catenin in fibroblast-like synoviocytes (FLS). In addition, increased miR-663 induced the FLS proliferation and the expression MMP3 and fibronectin during disease development. Therefore, miR-663 can be considered as a critical regulator of RA pathogenesis and can be utilized for developing miRNA-based therapeutic agents for RA patients.<br /> (Copyright © 2015 European Federation of Immunological Societies. Published by Elsevier B.V. All rights reserved.)
- Subjects :
- 3' Untranslated Regions genetics
Adenomatous Polyposis Coli Protein biosynthesis
Adult
Arthritis, Rheumatoid pathology
Binding Sites genetics
Cell Line
Cell Proliferation
Female
Fibronectins biosynthesis
Humans
Interleukin-6 biosynthesis
Interleukin-8 biosynthesis
Male
Matrix Metalloproteinase 3 biosynthesis
MicroRNAs biosynthesis
Middle Aged
Synovial Membrane cytology
beta Catenin metabolism
Adenomatous Polyposis Coli Protein genetics
Arthritis, Rheumatoid genetics
MicroRNAs genetics
Synovial Membrane metabolism
Wnt Signaling Pathway genetics
Subjects
Details
- Language :
- English
- ISSN :
- 1879-0542
- Volume :
- 166
- Issue :
- 1
- Database :
- MEDLINE
- Journal :
- Immunology letters
- Publication Type :
- Academic Journal
- Accession number :
- 26028359
- Full Text :
- https://doi.org/10.1016/j.imlet.2015.05.011