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The lncRNA RP11-142A22.4 promotes adipogenesis by sponging miR-587 to modulate Wnt5β expression
Emerging evidence suggests that long noncoding RNAs (lncRNAs) play essential roles in the regulation of gene expression. However, the functional contributions of lncRNAs to adipogenesis remain largely unexplored. In this study, we investigated global changes in the expression patterns of lncRNAs in...
Autores principales: | , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group UK
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7305230/ https://www.ncbi.nlm.nih.gov/pubmed/32561739 http://dx.doi.org/10.1038/s41419-020-2550-9 |
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author | Zhang, Tongtong Liu, Hongtao Mao, Rui Yang, Huawu Zhang, Yuanchuan Zhang, Yu Guo, Pengsen Zhan, Dafang Xiang, Bin Liu, Yanjun |
author_facet | Zhang, Tongtong Liu, Hongtao Mao, Rui Yang, Huawu Zhang, Yuanchuan Zhang, Yu Guo, Pengsen Zhan, Dafang Xiang, Bin Liu, Yanjun |
author_sort | Zhang, Tongtong |
collection | PubMed |
description | Emerging evidence suggests that long noncoding RNAs (lncRNAs) play essential roles in the regulation of gene expression. However, the functional contributions of lncRNAs to adipogenesis remain largely unexplored. In this study, we investigated global changes in the expression patterns of lncRNAs in visceral adipose tissue and identified RP11-142A22.4 as a significantly upregulated lncRNA. In isolated preadipocytes, knockdown of RP11-142A22.4 inhibited differentiation and reduced C/EBP-α and PPAR-γ expression. Investigations of the underlying mechanisms revealed that RP11-142A22.4 contains a functional miR-587 binding site. Mutation of the binding sites for RP11-142A22.4 in miR-587 abolished the interaction, as indicated by a luciferase reporter assay. Furthermore, RP11-142A22.4 affected the expression of miR-587 and its target gene Wnt5β. Overexpression of miR-587 blocked the inhibitory effect of RP11-142A22.4 on preadipocyte differentiation. Moreover, the downregulation of miR-587 restored preadipocyte differentiation upon inhibition by RP11-142A22.4 silencing. Our results suggest that RP11-142A22.4 can control adipocyte differentiation via the miR-587/Wnt5β signaling pathway and serve as a potential target for obesity treatments. |
format | Online Article Text |
id | pubmed-7305230 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-73052302020-06-26 The lncRNA RP11-142A22.4 promotes adipogenesis by sponging miR-587 to modulate Wnt5β expression Zhang, Tongtong Liu, Hongtao Mao, Rui Yang, Huawu Zhang, Yuanchuan Zhang, Yu Guo, Pengsen Zhan, Dafang Xiang, Bin Liu, Yanjun Cell Death Dis Article Emerging evidence suggests that long noncoding RNAs (lncRNAs) play essential roles in the regulation of gene expression. However, the functional contributions of lncRNAs to adipogenesis remain largely unexplored. In this study, we investigated global changes in the expression patterns of lncRNAs in visceral adipose tissue and identified RP11-142A22.4 as a significantly upregulated lncRNA. In isolated preadipocytes, knockdown of RP11-142A22.4 inhibited differentiation and reduced C/EBP-α and PPAR-γ expression. Investigations of the underlying mechanisms revealed that RP11-142A22.4 contains a functional miR-587 binding site. Mutation of the binding sites for RP11-142A22.4 in miR-587 abolished the interaction, as indicated by a luciferase reporter assay. Furthermore, RP11-142A22.4 affected the expression of miR-587 and its target gene Wnt5β. Overexpression of miR-587 blocked the inhibitory effect of RP11-142A22.4 on preadipocyte differentiation. Moreover, the downregulation of miR-587 restored preadipocyte differentiation upon inhibition by RP11-142A22.4 silencing. Our results suggest that RP11-142A22.4 can control adipocyte differentiation via the miR-587/Wnt5β signaling pathway and serve as a potential target for obesity treatments. Nature Publishing Group UK 2020-06-19 /pmc/articles/PMC7305230/ /pubmed/32561739 http://dx.doi.org/10.1038/s41419-020-2550-9 Text en © The Author(s) 2020 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/. |
spellingShingle | Article Zhang, Tongtong Liu, Hongtao Mao, Rui Yang, Huawu Zhang, Yuanchuan Zhang, Yu Guo, Pengsen Zhan, Dafang Xiang, Bin Liu, Yanjun The lncRNA RP11-142A22.4 promotes adipogenesis by sponging miR-587 to modulate Wnt5β expression |
title | The lncRNA RP11-142A22.4 promotes adipogenesis by sponging miR-587 to modulate Wnt5β expression |
title_full | The lncRNA RP11-142A22.4 promotes adipogenesis by sponging miR-587 to modulate Wnt5β expression |
title_fullStr | The lncRNA RP11-142A22.4 promotes adipogenesis by sponging miR-587 to modulate Wnt5β expression |
title_full_unstemmed | The lncRNA RP11-142A22.4 promotes adipogenesis by sponging miR-587 to modulate Wnt5β expression |
title_short | The lncRNA RP11-142A22.4 promotes adipogenesis by sponging miR-587 to modulate Wnt5β expression |
title_sort | lncrna rp11-142a22.4 promotes adipogenesis by sponging mir-587 to modulate wnt5β expression |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7305230/ https://www.ncbi.nlm.nih.gov/pubmed/32561739 http://dx.doi.org/10.1038/s41419-020-2550-9 |
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