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N(6)-methyladenosine (m(6)A) methyltransferase METTL3-mediated LINC00680 accelerates osteoarthritis through m(6)A/SIRT1 manner
Increasing evidence suggest the biological roles of N(6)-methyladenosine (m(6)A) and long noncoding RNAs (lncRNAs) in the bone disease, especially osteoarthritis (OA). However, the interaction of m(6)A and lncRNA in osteoarthritis is still unclear. Here, we found that a m(6)A-related lncRNA LINC0068...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group UK
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9061755/ https://www.ncbi.nlm.nih.gov/pubmed/35501316 http://dx.doi.org/10.1038/s41420-022-00890-0 |
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author | Ren, Jiangdong Li, Yicheng Wuermanbieke, Shalitanati Hu, Shu Huang, Guangxin |
author_facet | Ren, Jiangdong Li, Yicheng Wuermanbieke, Shalitanati Hu, Shu Huang, Guangxin |
author_sort | Ren, Jiangdong |
collection | PubMed |
description | Increasing evidence suggest the biological roles of N(6)-methyladenosine (m(6)A) and long noncoding RNAs (lncRNAs) in the bone disease, especially osteoarthritis (OA). However, the interaction of m(6)A and lncRNA in osteoarthritis is still unclear. Here, we found that a m(6)A-related lncRNA LINC00680 upregulated in the OA tissue and IL-1β-induced isolated primary chondrocytes. Functionally, in IL-1β-induced chondrocytes, silencing of LINC00680 recovered the proliferation and repressed the extracellular matrix (ECM) degradation. Mechanistically, m(6)A methyltransferase METTL3 combined tithe the m(6)A site of LINC00680 to up-regulate its expression. Moreover, LINC00680 interacted with SIRT1 mRNA through binding at m(6)A site on SIRT1 mRNA 3′-UTR, thereby enhancing the stability of SIRT1 mRNA. Overall, these findings exhibited a role of LINC00680/m(6)A/SIRT1 mRNA complex in chondrocytes. Taken together, the present study intends to uncover the mechanism by which METTL3-mediated LINC00680 accelerates OA progression, which may provide novel insight for OA. |
format | Online Article Text |
id | pubmed-9061755 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-90617552022-05-04 N(6)-methyladenosine (m(6)A) methyltransferase METTL3-mediated LINC00680 accelerates osteoarthritis through m(6)A/SIRT1 manner Ren, Jiangdong Li, Yicheng Wuermanbieke, Shalitanati Hu, Shu Huang, Guangxin Cell Death Discov Article Increasing evidence suggest the biological roles of N(6)-methyladenosine (m(6)A) and long noncoding RNAs (lncRNAs) in the bone disease, especially osteoarthritis (OA). However, the interaction of m(6)A and lncRNA in osteoarthritis is still unclear. Here, we found that a m(6)A-related lncRNA LINC00680 upregulated in the OA tissue and IL-1β-induced isolated primary chondrocytes. Functionally, in IL-1β-induced chondrocytes, silencing of LINC00680 recovered the proliferation and repressed the extracellular matrix (ECM) degradation. Mechanistically, m(6)A methyltransferase METTL3 combined tithe the m(6)A site of LINC00680 to up-regulate its expression. Moreover, LINC00680 interacted with SIRT1 mRNA through binding at m(6)A site on SIRT1 mRNA 3′-UTR, thereby enhancing the stability of SIRT1 mRNA. Overall, these findings exhibited a role of LINC00680/m(6)A/SIRT1 mRNA complex in chondrocytes. Taken together, the present study intends to uncover the mechanism by which METTL3-mediated LINC00680 accelerates OA progression, which may provide novel insight for OA. Nature Publishing Group UK 2022-05-02 /pmc/articles/PMC9061755/ /pubmed/35501316 http://dx.doi.org/10.1038/s41420-022-00890-0 Text en © The Author(s) 2022 https://creativecommons.org/licenses/by/4.0/Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) . |
spellingShingle | Article Ren, Jiangdong Li, Yicheng Wuermanbieke, Shalitanati Hu, Shu Huang, Guangxin N(6)-methyladenosine (m(6)A) methyltransferase METTL3-mediated LINC00680 accelerates osteoarthritis through m(6)A/SIRT1 manner |
title | N(6)-methyladenosine (m(6)A) methyltransferase METTL3-mediated LINC00680 accelerates osteoarthritis through m(6)A/SIRT1 manner |
title_full | N(6)-methyladenosine (m(6)A) methyltransferase METTL3-mediated LINC00680 accelerates osteoarthritis through m(6)A/SIRT1 manner |
title_fullStr | N(6)-methyladenosine (m(6)A) methyltransferase METTL3-mediated LINC00680 accelerates osteoarthritis through m(6)A/SIRT1 manner |
title_full_unstemmed | N(6)-methyladenosine (m(6)A) methyltransferase METTL3-mediated LINC00680 accelerates osteoarthritis through m(6)A/SIRT1 manner |
title_short | N(6)-methyladenosine (m(6)A) methyltransferase METTL3-mediated LINC00680 accelerates osteoarthritis through m(6)A/SIRT1 manner |
title_sort | n(6)-methyladenosine (m(6)a) methyltransferase mettl3-mediated linc00680 accelerates osteoarthritis through m(6)a/sirt1 manner |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9061755/ https://www.ncbi.nlm.nih.gov/pubmed/35501316 http://dx.doi.org/10.1038/s41420-022-00890-0 |
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