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lncRNA MEG3 Suppresses the Progression of Ankylosis Spondylitis by Regulating the Let-7i/SOST Axis
Ankylosis spondylitis (AS) is a disease mainly characterized by sacroiliac joint and spinal attachment point inflammation. Long non-coding RNA (lncRNA) plays a key role in the progression of many diseases. However, few studies have been conducted on the function of lncRNA maternally expressed gene 3...
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Frontiers Media S.A.
2020
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7393269/ https://www.ncbi.nlm.nih.gov/pubmed/32793634 http://dx.doi.org/10.3389/fmolb.2020.00173 |
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author | Ma, Junjie Zhang, Xiaohua Zhang, Hongxing Chen, Hailong |
author_facet | Ma, Junjie Zhang, Xiaohua Zhang, Hongxing Chen, Hailong |
author_sort | Ma, Junjie |
collection | PubMed |
description | Ankylosis spondylitis (AS) is a disease mainly characterized by sacroiliac joint and spinal attachment point inflammation. Long non-coding RNA (lncRNA) plays a key role in the progression of many diseases. However, few studies have been conducted on the function of lncRNA maternally expressed gene 3 (MEG3) in AS. Quantitative real-time polymerase chain reaction (qRT-PCR) was used to measure the relative levels of MEG3, microRNA let-7i, sclerostin (SOST), and inflammatory cytokines. Dual-luciferase reporter assay, RNA immunoprecipitation (RIP) assay and biotin-labeled RNA pull-down assay were used to confirm the interaction between MEG3 and let-7i or let-7i and SOST. In addition, western blot (WB) analysis was performed to detect the protein levels of osteogenesis markers and SOST. The expression levels of MEG3 and SOST were decreased and let-7i was increased in AS patients. MEG3 could interact with let-7i in AS fibroblasts, and let-7i overexpression reversed the suppressive effect of MEG3 upregulation on the inflammation and bone formation of AS. Additionally, let-7i could target SOST, and SOST silencing reversed the inhibitory effect of let-7i inhibitor or MEG3 overexpression on the inflammation and bone formation of AS. Furthermore, SOST expression was positively regulated by MEG3, while was negatively regulated by let-7i. Our results revealed that lncRNA MEG3 promoted SOST expression to restrain the progression of AS by sponging let-7i, which provided a treatment target for AS. |
format | Online Article Text |
id | pubmed-7393269 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-73932692020-08-12 lncRNA MEG3 Suppresses the Progression of Ankylosis Spondylitis by Regulating the Let-7i/SOST Axis Ma, Junjie Zhang, Xiaohua Zhang, Hongxing Chen, Hailong Front Mol Biosci Molecular Biosciences Ankylosis spondylitis (AS) is a disease mainly characterized by sacroiliac joint and spinal attachment point inflammation. Long non-coding RNA (lncRNA) plays a key role in the progression of many diseases. However, few studies have been conducted on the function of lncRNA maternally expressed gene 3 (MEG3) in AS. Quantitative real-time polymerase chain reaction (qRT-PCR) was used to measure the relative levels of MEG3, microRNA let-7i, sclerostin (SOST), and inflammatory cytokines. Dual-luciferase reporter assay, RNA immunoprecipitation (RIP) assay and biotin-labeled RNA pull-down assay were used to confirm the interaction between MEG3 and let-7i or let-7i and SOST. In addition, western blot (WB) analysis was performed to detect the protein levels of osteogenesis markers and SOST. The expression levels of MEG3 and SOST were decreased and let-7i was increased in AS patients. MEG3 could interact with let-7i in AS fibroblasts, and let-7i overexpression reversed the suppressive effect of MEG3 upregulation on the inflammation and bone formation of AS. Additionally, let-7i could target SOST, and SOST silencing reversed the inhibitory effect of let-7i inhibitor or MEG3 overexpression on the inflammation and bone formation of AS. Furthermore, SOST expression was positively regulated by MEG3, while was negatively regulated by let-7i. Our results revealed that lncRNA MEG3 promoted SOST expression to restrain the progression of AS by sponging let-7i, which provided a treatment target for AS. Frontiers Media S.A. 2020-07-24 /pmc/articles/PMC7393269/ /pubmed/32793634 http://dx.doi.org/10.3389/fmolb.2020.00173 Text en Copyright © 2020 Ma, Zhang, Zhang and Chen. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. |
spellingShingle | Molecular Biosciences Ma, Junjie Zhang, Xiaohua Zhang, Hongxing Chen, Hailong lncRNA MEG3 Suppresses the Progression of Ankylosis Spondylitis by Regulating the Let-7i/SOST Axis |
title | lncRNA MEG3 Suppresses the Progression of Ankylosis Spondylitis by Regulating the Let-7i/SOST Axis |
title_full | lncRNA MEG3 Suppresses the Progression of Ankylosis Spondylitis by Regulating the Let-7i/SOST Axis |
title_fullStr | lncRNA MEG3 Suppresses the Progression of Ankylosis Spondylitis by Regulating the Let-7i/SOST Axis |
title_full_unstemmed | lncRNA MEG3 Suppresses the Progression of Ankylosis Spondylitis by Regulating the Let-7i/SOST Axis |
title_short | lncRNA MEG3 Suppresses the Progression of Ankylosis Spondylitis by Regulating the Let-7i/SOST Axis |
title_sort | lncrna meg3 suppresses the progression of ankylosis spondylitis by regulating the let-7i/sost axis |
topic | Molecular Biosciences |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7393269/ https://www.ncbi.nlm.nih.gov/pubmed/32793634 http://dx.doi.org/10.3389/fmolb.2020.00173 |
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