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Long noncoding RNA ATB promotes the epithelial−mesenchymal transition by upregulating the miR-200c/Twist1 axe and predicts poor prognosis in breast cancer
Recent studies indicate that the long noncoding RNA ATB (lncATB) can induce the epithelial−mesenchymal transition (EMT) in cancer cells, but the specific cellular targets of lncATB require further investigation. In the present study, the upregulation of lncATB in breast cancer cells was validated in...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Nature Publishing Group UK
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6281614/ https://www.ncbi.nlm.nih.gov/pubmed/30518916 http://dx.doi.org/10.1038/s41419-018-1210-9 |
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author | Li, Rong-Hui Chen, Min Liu, Jing Shao, Chang-Chun Guo, Cui-Ping Wei, Xiao-Long Li, Yao-Chen Huang, Wen-He Zhang, Guo-Jun |
author_facet | Li, Rong-Hui Chen, Min Liu, Jing Shao, Chang-Chun Guo, Cui-Ping Wei, Xiao-Long Li, Yao-Chen Huang, Wen-He Zhang, Guo-Jun |
author_sort | Li, Rong-Hui |
collection | PubMed |
description | Recent studies indicate that the long noncoding RNA ATB (lncATB) can induce the epithelial−mesenchymal transition (EMT) in cancer cells, but the specific cellular targets of lncATB require further investigation. In the present study, the upregulation of lncATB in breast cancer cells was validated in a TGF-β-induced EMT model. Gain- and loss-of-function studies demonstrated that lncATB enhanced cell migration, invasion and clonogenicity in vitro and in vivo. LncATB promoted the EMT by acting as a sponge for the miR-200 family and restoring Twist1 expression. Subsequently, the clinical significance of lncATB was investigated in a cohort of breast cancer patients (N = 131). Higher lncATB expression was correlated with increased nodal metastasis (P = 0.036) and advanced clinical stage (P = 0.011) as well as shorter disease-free survival (P = 0.043) and overall survival (P = 0.046). These findings define Twist1 as a major target of lncATB in the induction of the EMT and highlight lncATB as a biomarker in breast cancer patients. |
format | Online Article Text |
id | pubmed-6281614 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-62816142018-12-06 Long noncoding RNA ATB promotes the epithelial−mesenchymal transition by upregulating the miR-200c/Twist1 axe and predicts poor prognosis in breast cancer Li, Rong-Hui Chen, Min Liu, Jing Shao, Chang-Chun Guo, Cui-Ping Wei, Xiao-Long Li, Yao-Chen Huang, Wen-He Zhang, Guo-Jun Cell Death Dis Article Recent studies indicate that the long noncoding RNA ATB (lncATB) can induce the epithelial−mesenchymal transition (EMT) in cancer cells, but the specific cellular targets of lncATB require further investigation. In the present study, the upregulation of lncATB in breast cancer cells was validated in a TGF-β-induced EMT model. Gain- and loss-of-function studies demonstrated that lncATB enhanced cell migration, invasion and clonogenicity in vitro and in vivo. LncATB promoted the EMT by acting as a sponge for the miR-200 family and restoring Twist1 expression. Subsequently, the clinical significance of lncATB was investigated in a cohort of breast cancer patients (N = 131). Higher lncATB expression was correlated with increased nodal metastasis (P = 0.036) and advanced clinical stage (P = 0.011) as well as shorter disease-free survival (P = 0.043) and overall survival (P = 0.046). These findings define Twist1 as a major target of lncATB in the induction of the EMT and highlight lncATB as a biomarker in breast cancer patients. Nature Publishing Group UK 2018-12-05 /pmc/articles/PMC6281614/ /pubmed/30518916 http://dx.doi.org/10.1038/s41419-018-1210-9 Text en © The Author(s) 2018 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 Li, Rong-Hui Chen, Min Liu, Jing Shao, Chang-Chun Guo, Cui-Ping Wei, Xiao-Long Li, Yao-Chen Huang, Wen-He Zhang, Guo-Jun Long noncoding RNA ATB promotes the epithelial−mesenchymal transition by upregulating the miR-200c/Twist1 axe and predicts poor prognosis in breast cancer |
title | Long noncoding RNA ATB promotes the epithelial−mesenchymal transition by upregulating the miR-200c/Twist1 axe and predicts poor prognosis in breast cancer |
title_full | Long noncoding RNA ATB promotes the epithelial−mesenchymal transition by upregulating the miR-200c/Twist1 axe and predicts poor prognosis in breast cancer |
title_fullStr | Long noncoding RNA ATB promotes the epithelial−mesenchymal transition by upregulating the miR-200c/Twist1 axe and predicts poor prognosis in breast cancer |
title_full_unstemmed | Long noncoding RNA ATB promotes the epithelial−mesenchymal transition by upregulating the miR-200c/Twist1 axe and predicts poor prognosis in breast cancer |
title_short | Long noncoding RNA ATB promotes the epithelial−mesenchymal transition by upregulating the miR-200c/Twist1 axe and predicts poor prognosis in breast cancer |
title_sort | long noncoding rna atb promotes the epithelial−mesenchymal transition by upregulating the mir-200c/twist1 axe and predicts poor prognosis in breast cancer |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6281614/ https://www.ncbi.nlm.nih.gov/pubmed/30518916 http://dx.doi.org/10.1038/s41419-018-1210-9 |
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