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Down-regulation of FTX promotes the differentiation of osteoclasts in osteoporosis through the Notch1 signaling pathway by targeting miR-137
BACKGROUND: Osteoporosis (OP) is one of the commonly seen bone diseases with low bone mineral densities and trauma fractures. Accumulative studies have demonstrated that the occurrence of OP is closely related to osteoclasts differentiation. LncRNA FTX has been demonstrated to inhibit the developmen...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7359489/ https://www.ncbi.nlm.nih.gov/pubmed/32660465 http://dx.doi.org/10.1186/s12891-020-03458-0 |
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author | Yu, Yingfeng Yao, Peiquan Wang, Zhikun Xie, Wenwei |
author_facet | Yu, Yingfeng Yao, Peiquan Wang, Zhikun Xie, Wenwei |
author_sort | Yu, Yingfeng |
collection | PubMed |
description | BACKGROUND: Osteoporosis (OP) is one of the commonly seen bone diseases with low bone mineral densities and trauma fractures. Accumulative studies have demonstrated that the occurrence of OP is closely related to osteoclasts differentiation. LncRNA FTX has been demonstrated to inhibit the development of some human cancers. However, its potential functions in human OP remains to be elusive. METHODS: The expressions of FTX and miR-137 in bone and serum samples of patients with or without OP were measured. Bioinformatics analysis, RIP assays and luciferase reporter assays were performed to examine the upstream and downstream transactional factors of miR-137. Functional assays were conducted to check the roles of the Notching1 signaling pathway OP. RESULTS: FTX was suppressed in OP samples and serums, however, miR-137 was greatly elevated. FTX reduced osteoclast-genesis and inhibited osteogenic differentiation by targeting miR-137. This also inhibited the Notch1 signaling pathway. CONCLUSION: Our experiments and results pointed out that lncRNA FTX up-regulated miR-137 in OP through the Notch1 signaling pathway. |
format | Online Article Text |
id | pubmed-7359489 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-73594892020-07-17 Down-regulation of FTX promotes the differentiation of osteoclasts in osteoporosis through the Notch1 signaling pathway by targeting miR-137 Yu, Yingfeng Yao, Peiquan Wang, Zhikun Xie, Wenwei BMC Musculoskelet Disord Research Article BACKGROUND: Osteoporosis (OP) is one of the commonly seen bone diseases with low bone mineral densities and trauma fractures. Accumulative studies have demonstrated that the occurrence of OP is closely related to osteoclasts differentiation. LncRNA FTX has been demonstrated to inhibit the development of some human cancers. However, its potential functions in human OP remains to be elusive. METHODS: The expressions of FTX and miR-137 in bone and serum samples of patients with or without OP were measured. Bioinformatics analysis, RIP assays and luciferase reporter assays were performed to examine the upstream and downstream transactional factors of miR-137. Functional assays were conducted to check the roles of the Notching1 signaling pathway OP. RESULTS: FTX was suppressed in OP samples and serums, however, miR-137 was greatly elevated. FTX reduced osteoclast-genesis and inhibited osteogenic differentiation by targeting miR-137. This also inhibited the Notch1 signaling pathway. CONCLUSION: Our experiments and results pointed out that lncRNA FTX up-regulated miR-137 in OP through the Notch1 signaling pathway. BioMed Central 2020-07-13 /pmc/articles/PMC7359489/ /pubmed/32660465 http://dx.doi.org/10.1186/s12891-020-03458-0 Text en © The Author(s) 2020 Open AccessThis 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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data. |
spellingShingle | Research Article Yu, Yingfeng Yao, Peiquan Wang, Zhikun Xie, Wenwei Down-regulation of FTX promotes the differentiation of osteoclasts in osteoporosis through the Notch1 signaling pathway by targeting miR-137 |
title | Down-regulation of FTX promotes the differentiation of osteoclasts in osteoporosis through the Notch1 signaling pathway by targeting miR-137 |
title_full | Down-regulation of FTX promotes the differentiation of osteoclasts in osteoporosis through the Notch1 signaling pathway by targeting miR-137 |
title_fullStr | Down-regulation of FTX promotes the differentiation of osteoclasts in osteoporosis through the Notch1 signaling pathway by targeting miR-137 |
title_full_unstemmed | Down-regulation of FTX promotes the differentiation of osteoclasts in osteoporosis through the Notch1 signaling pathway by targeting miR-137 |
title_short | Down-regulation of FTX promotes the differentiation of osteoclasts in osteoporosis through the Notch1 signaling pathway by targeting miR-137 |
title_sort | down-regulation of ftx promotes the differentiation of osteoclasts in osteoporosis through the notch1 signaling pathway by targeting mir-137 |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7359489/ https://www.ncbi.nlm.nih.gov/pubmed/32660465 http://dx.doi.org/10.1186/s12891-020-03458-0 |
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