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The activation of microRNA-520h–associated TGF-β1/c-Myb/Smad7 axis promotes epithelial ovarian cancer progression
Among the gynaecological cancers, epithelial ovarian cancer (EOC) has the highest lethality because of the high incidence of tumour progression and metastasis. Exploration of the detailed mechanisms underlying EOC metastasis and the identification of crucial targets is important to better estimate t...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group UK
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6115398/ https://www.ncbi.nlm.nih.gov/pubmed/30158641 http://dx.doi.org/10.1038/s41419-018-0946-6 |
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author | Zhang, Jing Liu, Wenxue Shen, Fangqian Ma, Xiaoling Liu, Xiaorui Tian, Fuju Zeng, Weihong Xi, Xiaowei Lin, Yi |
author_facet | Zhang, Jing Liu, Wenxue Shen, Fangqian Ma, Xiaoling Liu, Xiaorui Tian, Fuju Zeng, Weihong Xi, Xiaowei Lin, Yi |
author_sort | Zhang, Jing |
collection | PubMed |
description | Among the gynaecological cancers, epithelial ovarian cancer (EOC) has the highest lethality because of the high incidence of tumour progression and metastasis. Exploration of the detailed mechanisms underlying EOC metastasis and the identification of crucial targets is important to better estimate the prognosis and improve the treatment of this disease. The present study aimed to identify the role of miR-520h in the prognosis of patients with EOC, and the mechanisms of its involvement in EOC progression. We showed that miR-520h was upregulated in 116 patients with EOC, especially in those with advanced-stage disease, and high miR-520h expression predicted poor outcome. Furthermore, ectopic expression of miR-520h enhanced EOC cell proliferation, migration and invasion, and induced epithelial–mesenchymal transition in vitro and in vivo. miR-520h promoted EOC progression by downregulating Smad7, and subsequently activating the TGF-β signalling pathway. Most importantly, TGF-β1 stimulation increased miR-520h expression in EOC cells by upregulating its transcription factor c-Myb. In conclusion, we described the role of the TGF-β1/c-Myb/miR-520h/Smad7 axis in EOC metastasis, and highlighted the possible use of miR-520h as a prognostic marker for EOC. |
format | Online Article Text |
id | pubmed-6115398 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-61153982018-08-30 The activation of microRNA-520h–associated TGF-β1/c-Myb/Smad7 axis promotes epithelial ovarian cancer progression Zhang, Jing Liu, Wenxue Shen, Fangqian Ma, Xiaoling Liu, Xiaorui Tian, Fuju Zeng, Weihong Xi, Xiaowei Lin, Yi Cell Death Dis Article Among the gynaecological cancers, epithelial ovarian cancer (EOC) has the highest lethality because of the high incidence of tumour progression and metastasis. Exploration of the detailed mechanisms underlying EOC metastasis and the identification of crucial targets is important to better estimate the prognosis and improve the treatment of this disease. The present study aimed to identify the role of miR-520h in the prognosis of patients with EOC, and the mechanisms of its involvement in EOC progression. We showed that miR-520h was upregulated in 116 patients with EOC, especially in those with advanced-stage disease, and high miR-520h expression predicted poor outcome. Furthermore, ectopic expression of miR-520h enhanced EOC cell proliferation, migration and invasion, and induced epithelial–mesenchymal transition in vitro and in vivo. miR-520h promoted EOC progression by downregulating Smad7, and subsequently activating the TGF-β signalling pathway. Most importantly, TGF-β1 stimulation increased miR-520h expression in EOC cells by upregulating its transcription factor c-Myb. In conclusion, we described the role of the TGF-β1/c-Myb/miR-520h/Smad7 axis in EOC metastasis, and highlighted the possible use of miR-520h as a prognostic marker for EOC. Nature Publishing Group UK 2018-08-29 /pmc/articles/PMC6115398/ /pubmed/30158641 http://dx.doi.org/10.1038/s41419-018-0946-6 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 Zhang, Jing Liu, Wenxue Shen, Fangqian Ma, Xiaoling Liu, Xiaorui Tian, Fuju Zeng, Weihong Xi, Xiaowei Lin, Yi The activation of microRNA-520h–associated TGF-β1/c-Myb/Smad7 axis promotes epithelial ovarian cancer progression |
title | The activation of microRNA-520h–associated TGF-β1/c-Myb/Smad7 axis promotes epithelial ovarian cancer progression |
title_full | The activation of microRNA-520h–associated TGF-β1/c-Myb/Smad7 axis promotes epithelial ovarian cancer progression |
title_fullStr | The activation of microRNA-520h–associated TGF-β1/c-Myb/Smad7 axis promotes epithelial ovarian cancer progression |
title_full_unstemmed | The activation of microRNA-520h–associated TGF-β1/c-Myb/Smad7 axis promotes epithelial ovarian cancer progression |
title_short | The activation of microRNA-520h–associated TGF-β1/c-Myb/Smad7 axis promotes epithelial ovarian cancer progression |
title_sort | activation of microrna-520h–associated tgf-β1/c-myb/smad7 axis promotes epithelial ovarian cancer progression |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6115398/ https://www.ncbi.nlm.nih.gov/pubmed/30158641 http://dx.doi.org/10.1038/s41419-018-0946-6 |
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