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Zeylenone represses the progress of human prostate cancer by downregulating the Wnt/β-catenin pathway
Prostate cancer (PCa) is one of the most common types of cancer in the urinary system in men. Zeylenone (Zey), a naturally occurring cyclohexene oxide, has an anticancer effect. In the present study, the role and potential mechanism of Zey in PCa were examined. The proliferative, invasive and migrat...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6236222/ https://www.ncbi.nlm.nih.gov/pubmed/30365080 http://dx.doi.org/10.3892/mmr.2018.9564 |
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author | Zeng, Shaohua Zhu, Baoyi Zeng, Jun Wu, Wenqi Jiang, Chonghe |
author_facet | Zeng, Shaohua Zhu, Baoyi Zeng, Jun Wu, Wenqi Jiang, Chonghe |
author_sort | Zeng, Shaohua |
collection | PubMed |
description | Prostate cancer (PCa) is one of the most common types of cancer in the urinary system in men. Zeylenone (Zey), a naturally occurring cyclohexene oxide, has an anticancer effect. In the present study, the role and potential mechanism of Zey in PCa were examined. The proliferative, invasive and migratory capacities of DU145 cells were analyzed using Cell Counting Kit-8, transwell and wound healing assays, respectively. The expression levels of matrix metalloproteinase (MMP)-2 and MMP-9 were determined with an ELISA. Reverse transcription-quantitative polymerase chain reaction and western blotting assays were performed to evaluate the expression levels of extracellular matrix, epithelial-mesenchymal transition and Wnt/β-catenin pathway-associated factors. In the present study, it was observed that Zey not only suppressed the viability of DU145 cells; however, it additionally attenuated the invasive and migratory capacities of cells in a concentration-dependent manner. Treatment of Zey decreased the expression levels of MMP-2, MMP-9 and fibronectin-1; whereas, it increased tissue inhibitor of metalloproteinases-1 and collagen-1 expression levels. Additionally, the vimentin expression level was downregulated, however, the epithelial-cadherin expression level was upregulated in cells treated with Zey. Furthermore, Zey decreased the expression levels of wnt5a, β-catenin and cyclin D1. In conclusion, the present results demonstrated that Zey decreased the viability and metastasis of human PCa cells (DU145), via the Wnt/β-catenin signaling pathway. Therefore, Zey may be applied as a novel drug for treating PCa in the future. |
format | Online Article Text |
id | pubmed-6236222 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | D.A. Spandidos |
record_format | MEDLINE/PubMed |
spelling | pubmed-62362222018-11-19 Zeylenone represses the progress of human prostate cancer by downregulating the Wnt/β-catenin pathway Zeng, Shaohua Zhu, Baoyi Zeng, Jun Wu, Wenqi Jiang, Chonghe Mol Med Rep Articles Prostate cancer (PCa) is one of the most common types of cancer in the urinary system in men. Zeylenone (Zey), a naturally occurring cyclohexene oxide, has an anticancer effect. In the present study, the role and potential mechanism of Zey in PCa were examined. The proliferative, invasive and migratory capacities of DU145 cells were analyzed using Cell Counting Kit-8, transwell and wound healing assays, respectively. The expression levels of matrix metalloproteinase (MMP)-2 and MMP-9 were determined with an ELISA. Reverse transcription-quantitative polymerase chain reaction and western blotting assays were performed to evaluate the expression levels of extracellular matrix, epithelial-mesenchymal transition and Wnt/β-catenin pathway-associated factors. In the present study, it was observed that Zey not only suppressed the viability of DU145 cells; however, it additionally attenuated the invasive and migratory capacities of cells in a concentration-dependent manner. Treatment of Zey decreased the expression levels of MMP-2, MMP-9 and fibronectin-1; whereas, it increased tissue inhibitor of metalloproteinases-1 and collagen-1 expression levels. Additionally, the vimentin expression level was downregulated, however, the epithelial-cadherin expression level was upregulated in cells treated with Zey. Furthermore, Zey decreased the expression levels of wnt5a, β-catenin and cyclin D1. In conclusion, the present results demonstrated that Zey decreased the viability and metastasis of human PCa cells (DU145), via the Wnt/β-catenin signaling pathway. Therefore, Zey may be applied as a novel drug for treating PCa in the future. D.A. Spandidos 2018-12 2018-10-17 /pmc/articles/PMC6236222/ /pubmed/30365080 http://dx.doi.org/10.3892/mmr.2018.9564 Text en Copyright: © Zeng 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 Zeng, Shaohua Zhu, Baoyi Zeng, Jun Wu, Wenqi Jiang, Chonghe Zeylenone represses the progress of human prostate cancer by downregulating the Wnt/β-catenin pathway |
title | Zeylenone represses the progress of human prostate cancer by downregulating the Wnt/β-catenin pathway |
title_full | Zeylenone represses the progress of human prostate cancer by downregulating the Wnt/β-catenin pathway |
title_fullStr | Zeylenone represses the progress of human prostate cancer by downregulating the Wnt/β-catenin pathway |
title_full_unstemmed | Zeylenone represses the progress of human prostate cancer by downregulating the Wnt/β-catenin pathway |
title_short | Zeylenone represses the progress of human prostate cancer by downregulating the Wnt/β-catenin pathway |
title_sort | zeylenone represses the progress of human prostate cancer by downregulating the wnt/β-catenin pathway |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6236222/ https://www.ncbi.nlm.nih.gov/pubmed/30365080 http://dx.doi.org/10.3892/mmr.2018.9564 |
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