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Astragalus polysaccharide inhibits breast cancer cell migration and invasion by regulating epithelial-mesenchymal transition via the Wnt/β-catenin signaling pathway
Epithelial-mesenchymal transition (EMT) serves an important role in tumor migration and invasion. Astragalus polysaccharide (APS), which is the main component of the traditional Chinese medicine Astragalus membranaceus, has been identified to display an antitumor effect. However, the effects and mec...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7057808/ https://www.ncbi.nlm.nih.gov/pubmed/32319619 http://dx.doi.org/10.3892/mmr.2020.10983 |
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author | Yang, Shuo Sun, Shuqin Xu, Wanqun Yu, Bangxu Wang, Guimei Wang, Haibo |
author_facet | Yang, Shuo Sun, Shuqin Xu, Wanqun Yu, Bangxu Wang, Guimei Wang, Haibo |
author_sort | Yang, Shuo |
collection | PubMed |
description | Epithelial-mesenchymal transition (EMT) serves an important role in tumor migration and invasion. Astragalus polysaccharide (APS), which is the main component of the traditional Chinese medicine Astragalus membranaceus, has been identified to display an antitumor effect. However, the effects and mechanisms of APS during breast cancer migration and invasion are not completely understood. The present study investigated whether APS inhibited breast cancer migration and invasion by modulating the EMT pathway. An MTT assay and a Ki67 immunofluorescence staining assay demonstrated that APS inhibited the proliferation of breast cancer cells. The results of the wound healing and Transwell Matrigel invasion assays suggested that APS decreased the migration and invasion of breast cancer cells. The western blotting and immunofluorescence analyses further demonstrated that APS had a regulatory effect on EMT-related molecules. APS decreased the expression levels of Snail and vimentin, but increased E-cadherin expression. APS also downregulated Wnt1, β-catenin and downstream target expression. Additionally, the present results suggested that APS decreased the proliferation, and EMT-mediated migration and invasion of cells by inhibiting the Wnt/β-catenin signaling pathway. The present study suggested that APS may serve as a promising therapeutic agent for breast cancer. |
format | Online Article Text |
id | pubmed-7057808 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | D.A. Spandidos |
record_format | MEDLINE/PubMed |
spelling | pubmed-70578082020-03-18 Astragalus polysaccharide inhibits breast cancer cell migration and invasion by regulating epithelial-mesenchymal transition via the Wnt/β-catenin signaling pathway Yang, Shuo Sun, Shuqin Xu, Wanqun Yu, Bangxu Wang, Guimei Wang, Haibo Mol Med Rep Articles Epithelial-mesenchymal transition (EMT) serves an important role in tumor migration and invasion. Astragalus polysaccharide (APS), which is the main component of the traditional Chinese medicine Astragalus membranaceus, has been identified to display an antitumor effect. However, the effects and mechanisms of APS during breast cancer migration and invasion are not completely understood. The present study investigated whether APS inhibited breast cancer migration and invasion by modulating the EMT pathway. An MTT assay and a Ki67 immunofluorescence staining assay demonstrated that APS inhibited the proliferation of breast cancer cells. The results of the wound healing and Transwell Matrigel invasion assays suggested that APS decreased the migration and invasion of breast cancer cells. The western blotting and immunofluorescence analyses further demonstrated that APS had a regulatory effect on EMT-related molecules. APS decreased the expression levels of Snail and vimentin, but increased E-cadherin expression. APS also downregulated Wnt1, β-catenin and downstream target expression. Additionally, the present results suggested that APS decreased the proliferation, and EMT-mediated migration and invasion of cells by inhibiting the Wnt/β-catenin signaling pathway. The present study suggested that APS may serve as a promising therapeutic agent for breast cancer. D.A. Spandidos 2020-04 2020-02-12 /pmc/articles/PMC7057808/ /pubmed/32319619 http://dx.doi.org/10.3892/mmr.2020.10983 Text en Copyright: © Yang 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 Yang, Shuo Sun, Shuqin Xu, Wanqun Yu, Bangxu Wang, Guimei Wang, Haibo Astragalus polysaccharide inhibits breast cancer cell migration and invasion by regulating epithelial-mesenchymal transition via the Wnt/β-catenin signaling pathway |
title | Astragalus polysaccharide inhibits breast cancer cell migration and invasion by regulating epithelial-mesenchymal transition via the Wnt/β-catenin signaling pathway |
title_full | Astragalus polysaccharide inhibits breast cancer cell migration and invasion by regulating epithelial-mesenchymal transition via the Wnt/β-catenin signaling pathway |
title_fullStr | Astragalus polysaccharide inhibits breast cancer cell migration and invasion by regulating epithelial-mesenchymal transition via the Wnt/β-catenin signaling pathway |
title_full_unstemmed | Astragalus polysaccharide inhibits breast cancer cell migration and invasion by regulating epithelial-mesenchymal transition via the Wnt/β-catenin signaling pathway |
title_short | Astragalus polysaccharide inhibits breast cancer cell migration and invasion by regulating epithelial-mesenchymal transition via the Wnt/β-catenin signaling pathway |
title_sort | astragalus polysaccharide inhibits breast cancer cell migration and invasion by regulating epithelial-mesenchymal transition via the wnt/β-catenin signaling pathway |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7057808/ https://www.ncbi.nlm.nih.gov/pubmed/32319619 http://dx.doi.org/10.3892/mmr.2020.10983 |
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