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Long non-coding RNA NEAT1 promotes pulmonary fibrosis by regulating the microRNA-455-3p/SMAD3 axis

Pulmonary fibrosis is an excessive repair response to tissue damage, triggering hyperplasia of fibrotic connective tissues; however, there is no effective treatment in a clinical setting. The purpose of the present study was to investigate the roles of long non-coding RNA nuclear enriched abundant t...

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Autores principales: Liu, Yuan, Lu, Fu-Ai, Wang, Le, Wang, Yong-Fu, Wu, Chun-Feng
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7845585/
https://www.ncbi.nlm.nih.gov/pubmed/33495816
http://dx.doi.org/10.3892/mmr.2021.11857
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author Liu, Yuan
Lu, Fu-Ai
Wang, Le
Wang, Yong-Fu
Wu, Chun-Feng
author_facet Liu, Yuan
Lu, Fu-Ai
Wang, Le
Wang, Yong-Fu
Wu, Chun-Feng
author_sort Liu, Yuan
collection PubMed
description Pulmonary fibrosis is an excessive repair response to tissue damage, triggering hyperplasia of fibrotic connective tissues; however, there is no effective treatment in a clinical setting. The purpose of the present study was to investigate the roles of long non-coding RNA nuclear enriched abundant transcript 1 (NEAT1) and microRNA-455-3p (miR-455-3p) were investigated in pulmonary fibrosis. In this study, the mRNA expression levels of NEAT1, miR-455-3p and SMAD3 in the HPAEpiC alveolar and BEAS-2B bronchial epithelial cell lines were determined using reverse transcription-quantitative PCR, while the markers of epithelial-mesenchymal transformation (EMT) and collagen production were determined using western blot analysis. A wound healing assay was performed to evaluate the migratory ability of the HPAEpiC and BEAS-2B cell lines. The interactions between NEAT1 and miR-455-3p or SMAD3 and miR-455-3p were validated using a luciferase reporter gene assay. The results showed that the mRNA expression levels of NEAT1 and SMAD3 were upregulated in the TGF-β1-treated HPAEpiC and BEAS-2B cell lines, while the mRNA expression level of miR-455-3p was significantly decreased. In addition, silencing NEAT1 effectively alleviated the migratory ability, EMT and collagen generation of the epithelial cells. Following these experiments, NEAT1 was identified as a sponge for miR-455-3p, and SMAD3 was a target gene of miR-455-3p. NEAT1 downregulation or miR-455-3p mimic inhibited the migratory ability, EMT and collagen production of the epithelial cells; however, the effects were reversed by the overexpression of SMAD3. Furthermore, NEAT1 knockdown reduced the expression level of SMAD3 by increasing the expression level of miR-455-3p to further inhibit the migratory ability, EMT and collagen production of epithelial cells.
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spelling pubmed-78455852021-02-02 Long non-coding RNA NEAT1 promotes pulmonary fibrosis by regulating the microRNA-455-3p/SMAD3 axis Liu, Yuan Lu, Fu-Ai Wang, Le Wang, Yong-Fu Wu, Chun-Feng Mol Med Rep Articles Pulmonary fibrosis is an excessive repair response to tissue damage, triggering hyperplasia of fibrotic connective tissues; however, there is no effective treatment in a clinical setting. The purpose of the present study was to investigate the roles of long non-coding RNA nuclear enriched abundant transcript 1 (NEAT1) and microRNA-455-3p (miR-455-3p) were investigated in pulmonary fibrosis. In this study, the mRNA expression levels of NEAT1, miR-455-3p and SMAD3 in the HPAEpiC alveolar and BEAS-2B bronchial epithelial cell lines were determined using reverse transcription-quantitative PCR, while the markers of epithelial-mesenchymal transformation (EMT) and collagen production were determined using western blot analysis. A wound healing assay was performed to evaluate the migratory ability of the HPAEpiC and BEAS-2B cell lines. The interactions between NEAT1 and miR-455-3p or SMAD3 and miR-455-3p were validated using a luciferase reporter gene assay. The results showed that the mRNA expression levels of NEAT1 and SMAD3 were upregulated in the TGF-β1-treated HPAEpiC and BEAS-2B cell lines, while the mRNA expression level of miR-455-3p was significantly decreased. In addition, silencing NEAT1 effectively alleviated the migratory ability, EMT and collagen generation of the epithelial cells. Following these experiments, NEAT1 was identified as a sponge for miR-455-3p, and SMAD3 was a target gene of miR-455-3p. NEAT1 downregulation or miR-455-3p mimic inhibited the migratory ability, EMT and collagen production of the epithelial cells; however, the effects were reversed by the overexpression of SMAD3. Furthermore, NEAT1 knockdown reduced the expression level of SMAD3 by increasing the expression level of miR-455-3p to further inhibit the migratory ability, EMT and collagen production of epithelial cells. D.A. Spandidos 2021-03 2021-01-20 /pmc/articles/PMC7845585/ /pubmed/33495816 http://dx.doi.org/10.3892/mmr.2021.11857 Text en Copyright: © Liu et al. This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.
spellingShingle Articles
Liu, Yuan
Lu, Fu-Ai
Wang, Le
Wang, Yong-Fu
Wu, Chun-Feng
Long non-coding RNA NEAT1 promotes pulmonary fibrosis by regulating the microRNA-455-3p/SMAD3 axis
title Long non-coding RNA NEAT1 promotes pulmonary fibrosis by regulating the microRNA-455-3p/SMAD3 axis
title_full Long non-coding RNA NEAT1 promotes pulmonary fibrosis by regulating the microRNA-455-3p/SMAD3 axis
title_fullStr Long non-coding RNA NEAT1 promotes pulmonary fibrosis by regulating the microRNA-455-3p/SMAD3 axis
title_full_unstemmed Long non-coding RNA NEAT1 promotes pulmonary fibrosis by regulating the microRNA-455-3p/SMAD3 axis
title_short Long non-coding RNA NEAT1 promotes pulmonary fibrosis by regulating the microRNA-455-3p/SMAD3 axis
title_sort long non-coding rna neat1 promotes pulmonary fibrosis by regulating the microrna-455-3p/smad3 axis
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7845585/
https://www.ncbi.nlm.nih.gov/pubmed/33495816
http://dx.doi.org/10.3892/mmr.2021.11857
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