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ZMYND10, an epigenetically regulated tumor suppressor, exerts tumor-suppressive functions via miR145-5p/NEDD9 axis in breast cancer
BACKGROUND: Recent studies suggested that ZMYND10 is a potential tumor suppressor gene in multiple tumor types. However, the mechanism by which ZMYND10 inhibits breast cancer remains unclear. Here, we investigated the role and mechanism of ZMYND10 in breast cancer inhibition. RESULTS: ZMYND10 was dr...
Autores principales: | , , , , , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6894283/ https://www.ncbi.nlm.nih.gov/pubmed/31801619 http://dx.doi.org/10.1186/s13148-019-0785-z |
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author | Wang, Yan Dan, Liangying Li, Qianqian Li, Lili Zhong, Lan Shao, Bianfei Yu, Fang He, Sanxiu Tian, Shaorong He, Jin Xiao, Qian Putti, Thomas C. He, Xiaoqian Feng, Yixiao Lin, Yong Xiang, Tingxiu |
author_facet | Wang, Yan Dan, Liangying Li, Qianqian Li, Lili Zhong, Lan Shao, Bianfei Yu, Fang He, Sanxiu Tian, Shaorong He, Jin Xiao, Qian Putti, Thomas C. He, Xiaoqian Feng, Yixiao Lin, Yong Xiang, Tingxiu |
author_sort | Wang, Yan |
collection | PubMed |
description | BACKGROUND: Recent studies suggested that ZMYND10 is a potential tumor suppressor gene in multiple tumor types. However, the mechanism by which ZMYND10 inhibits breast cancer remains unclear. Here, we investigated the role and mechanism of ZMYND10 in breast cancer inhibition. RESULTS: ZMYND10 was dramatically reduced in multiple breast cancer cell lines and tissues, which was associated with promoter hypermethylation. Ectopic expression of ZMYND10 in silenced breast cancer cells induced cell apoptosis while suppressed cell growth, cell migration and invasion in vitro, and xenograft tumor growth in vivo. Furthermore, molecular mechanism studies indicated that ZMYND10 enhances expression of miR145-5p, which suppresses the expression of NEDD9 protein through directly targeting the 3'-untranslated region of NEDD9 mRNA. CONCLUSIONS: Results from this study show that ZMYND10 suppresses breast cancer tumorigenicity by inhibiting the miR145-5p/NEDD9 signaling pathway. This novel discovered signaling pathway may be a valid target for small molecules that might help to develop new therapies to better inhibit the breast cancer metastasis. |
format | Online Article Text |
id | pubmed-6894283 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-68942832019-12-11 ZMYND10, an epigenetically regulated tumor suppressor, exerts tumor-suppressive functions via miR145-5p/NEDD9 axis in breast cancer Wang, Yan Dan, Liangying Li, Qianqian Li, Lili Zhong, Lan Shao, Bianfei Yu, Fang He, Sanxiu Tian, Shaorong He, Jin Xiao, Qian Putti, Thomas C. He, Xiaoqian Feng, Yixiao Lin, Yong Xiang, Tingxiu Clin Epigenetics Research BACKGROUND: Recent studies suggested that ZMYND10 is a potential tumor suppressor gene in multiple tumor types. However, the mechanism by which ZMYND10 inhibits breast cancer remains unclear. Here, we investigated the role and mechanism of ZMYND10 in breast cancer inhibition. RESULTS: ZMYND10 was dramatically reduced in multiple breast cancer cell lines and tissues, which was associated with promoter hypermethylation. Ectopic expression of ZMYND10 in silenced breast cancer cells induced cell apoptosis while suppressed cell growth, cell migration and invasion in vitro, and xenograft tumor growth in vivo. Furthermore, molecular mechanism studies indicated that ZMYND10 enhances expression of miR145-5p, which suppresses the expression of NEDD9 protein through directly targeting the 3'-untranslated region of NEDD9 mRNA. CONCLUSIONS: Results from this study show that ZMYND10 suppresses breast cancer tumorigenicity by inhibiting the miR145-5p/NEDD9 signaling pathway. This novel discovered signaling pathway may be a valid target for small molecules that might help to develop new therapies to better inhibit the breast cancer metastasis. BioMed Central 2019-12-04 /pmc/articles/PMC6894283/ /pubmed/31801619 http://dx.doi.org/10.1186/s13148-019-0785-z Text en © The Author(s). 2019 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided 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 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. |
spellingShingle | Research Wang, Yan Dan, Liangying Li, Qianqian Li, Lili Zhong, Lan Shao, Bianfei Yu, Fang He, Sanxiu Tian, Shaorong He, Jin Xiao, Qian Putti, Thomas C. He, Xiaoqian Feng, Yixiao Lin, Yong Xiang, Tingxiu ZMYND10, an epigenetically regulated tumor suppressor, exerts tumor-suppressive functions via miR145-5p/NEDD9 axis in breast cancer |
title | ZMYND10, an epigenetically regulated tumor suppressor, exerts tumor-suppressive functions via miR145-5p/NEDD9 axis in breast cancer |
title_full | ZMYND10, an epigenetically regulated tumor suppressor, exerts tumor-suppressive functions via miR145-5p/NEDD9 axis in breast cancer |
title_fullStr | ZMYND10, an epigenetically regulated tumor suppressor, exerts tumor-suppressive functions via miR145-5p/NEDD9 axis in breast cancer |
title_full_unstemmed | ZMYND10, an epigenetically regulated tumor suppressor, exerts tumor-suppressive functions via miR145-5p/NEDD9 axis in breast cancer |
title_short | ZMYND10, an epigenetically regulated tumor suppressor, exerts tumor-suppressive functions via miR145-5p/NEDD9 axis in breast cancer |
title_sort | zmynd10, an epigenetically regulated tumor suppressor, exerts tumor-suppressive functions via mir145-5p/nedd9 axis in breast cancer |
topic | Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6894283/ https://www.ncbi.nlm.nih.gov/pubmed/31801619 http://dx.doi.org/10.1186/s13148-019-0785-z |
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