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DNER promotes epithelial–mesenchymal transition and prevents chemosensitivity through the Wnt/β-catenin pathway in breast cancer

Breast cancer (BC) is the most common malignant tumour in women worldwide, and one of the most common fatal tumours in women. Delta/Notch-like epidermal growth factor (EGF)-related receptor (DNER) is a transmembrane protein involved in the development of tumours. The role and potential mechanism of...

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Autores principales: Wang, Zhong, Li, Zhiyu, Wu, Qi, Li, Chenyuan, Li, Juanjuan, Zhang, Yimin, Wang, Changhua, Sun, Si, Sun, Shengrong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7434780/
https://www.ncbi.nlm.nih.gov/pubmed/32811806
http://dx.doi.org/10.1038/s41419-020-02903-1
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author Wang, Zhong
Li, Zhiyu
Wu, Qi
Li, Chenyuan
Li, Juanjuan
Zhang, Yimin
Wang, Changhua
Sun, Si
Sun, Shengrong
author_facet Wang, Zhong
Li, Zhiyu
Wu, Qi
Li, Chenyuan
Li, Juanjuan
Zhang, Yimin
Wang, Changhua
Sun, Si
Sun, Shengrong
author_sort Wang, Zhong
collection PubMed
description Breast cancer (BC) is the most common malignant tumour in women worldwide, and one of the most common fatal tumours in women. Delta/Notch-like epidermal growth factor (EGF)-related receptor (DNER) is a transmembrane protein involved in the development of tumours. The role and potential mechanism of DNER in epithelial–mesenchymal transition (EMT) and apoptosis in BC are not fully understood. We find that DNER is overexpressed in BC tissue, especially triple-negative breast cancer (TNBC) tissue, and related to the survival of BC and TNBC patients. In addition, DNER regulates cell EMT to enhance the proliferation and metastasis of BC cells via the Wnt/β-catenin pathway in vitro and in vivo. Moreover, the expression levels of β-catenin and DNER in BD tissue are positively correlated. The simultaneously high expression of DNER and β-catenin contributes to poor prognosis in BC patients. Finally, DNER protects BC cells from epirubicin-induced growth inhibition and apoptosis via the Wnt/β-catenin pathway. In conclusion, these results suggest that DNER induces EMT and prevents apoptosis by the Wnt/β-catenin pathway, ultimately promoting the malignant progression of BC. In conclusion, our study demonstrates that DNER functions as an oncogene and potentially valuable therapeutic target for BC.
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spelling pubmed-74347802020-08-27 DNER promotes epithelial–mesenchymal transition and prevents chemosensitivity through the Wnt/β-catenin pathway in breast cancer Wang, Zhong Li, Zhiyu Wu, Qi Li, Chenyuan Li, Juanjuan Zhang, Yimin Wang, Changhua Sun, Si Sun, Shengrong Cell Death Dis Article Breast cancer (BC) is the most common malignant tumour in women worldwide, and one of the most common fatal tumours in women. Delta/Notch-like epidermal growth factor (EGF)-related receptor (DNER) is a transmembrane protein involved in the development of tumours. The role and potential mechanism of DNER in epithelial–mesenchymal transition (EMT) and apoptosis in BC are not fully understood. We find that DNER is overexpressed in BC tissue, especially triple-negative breast cancer (TNBC) tissue, and related to the survival of BC and TNBC patients. In addition, DNER regulates cell EMT to enhance the proliferation and metastasis of BC cells via the Wnt/β-catenin pathway in vitro and in vivo. Moreover, the expression levels of β-catenin and DNER in BD tissue are positively correlated. The simultaneously high expression of DNER and β-catenin contributes to poor prognosis in BC patients. Finally, DNER protects BC cells from epirubicin-induced growth inhibition and apoptosis via the Wnt/β-catenin pathway. In conclusion, these results suggest that DNER induces EMT and prevents apoptosis by the Wnt/β-catenin pathway, ultimately promoting the malignant progression of BC. In conclusion, our study demonstrates that DNER functions as an oncogene and potentially valuable therapeutic target for BC. Nature Publishing Group UK 2020-08-18 /pmc/articles/PMC7434780/ /pubmed/32811806 http://dx.doi.org/10.1038/s41419-020-02903-1 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
Wang, Zhong
Li, Zhiyu
Wu, Qi
Li, Chenyuan
Li, Juanjuan
Zhang, Yimin
Wang, Changhua
Sun, Si
Sun, Shengrong
DNER promotes epithelial–mesenchymal transition and prevents chemosensitivity through the Wnt/β-catenin pathway in breast cancer
title DNER promotes epithelial–mesenchymal transition and prevents chemosensitivity through the Wnt/β-catenin pathway in breast cancer
title_full DNER promotes epithelial–mesenchymal transition and prevents chemosensitivity through the Wnt/β-catenin pathway in breast cancer
title_fullStr DNER promotes epithelial–mesenchymal transition and prevents chemosensitivity through the Wnt/β-catenin pathway in breast cancer
title_full_unstemmed DNER promotes epithelial–mesenchymal transition and prevents chemosensitivity through the Wnt/β-catenin pathway in breast cancer
title_short DNER promotes epithelial–mesenchymal transition and prevents chemosensitivity through the Wnt/β-catenin pathway in breast cancer
title_sort dner promotes epithelial–mesenchymal transition and prevents chemosensitivity through the wnt/β-catenin pathway in breast cancer
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7434780/
https://www.ncbi.nlm.nih.gov/pubmed/32811806
http://dx.doi.org/10.1038/s41419-020-02903-1
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