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1α,25(OH)(2)D(3) Suppresses the Migration of Ovarian Cancer SKOV-3 Cells through the Inhibition of Epithelial–Mesenchymal Transition
Ovarian cancer is the most lethal gynecological malignancy due to its high metastatic ability. Epithelial-mesenchymal transition (EMT) is essential during both follicular rupture and epithelium regeneration. However, it may also accelerate the progression of ovarian carcinomas. Experimental studies...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2016
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5000682/ https://www.ncbi.nlm.nih.gov/pubmed/27548154 http://dx.doi.org/10.3390/ijms17081285 |
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author | Hou, Yong-Feng Gao, Si-Hai Wang, Ping Zhang, He-Mei Liu, Li-Zhi Ye, Meng-Xuan Zhou, Guang-Ming Zhang, Zeng-Li Li, Bing-Yan |
author_facet | Hou, Yong-Feng Gao, Si-Hai Wang, Ping Zhang, He-Mei Liu, Li-Zhi Ye, Meng-Xuan Zhou, Guang-Ming Zhang, Zeng-Li Li, Bing-Yan |
author_sort | Hou, Yong-Feng |
collection | PubMed |
description | Ovarian cancer is the most lethal gynecological malignancy due to its high metastatic ability. Epithelial-mesenchymal transition (EMT) is essential during both follicular rupture and epithelium regeneration. However, it may also accelerate the progression of ovarian carcinomas. Experimental studies have found that 1α,25-dihydroxyvitamin-D3 [1α,25(OH)(2)D(3)] can inhibit the proliferation of ovarian cancer cells. In this study, we investigated whether 1α,25(OH)(2)D(3) could inhibit the migration of ovarian cancer cells via regulating EMT. We established a model of transient transforming growth factor-β1(TGF-β1)-induced EMT in human ovarian adenocarcinoma cell line SKOV-3 cells. Results showed that, compared with control, 1α,25(OH)(2)D(3) not only inhibited the migration and the invasion of SKOV-3 cells, but also promoted the acquisition of an epithelial phenotype of SKOV-3 cells treated with TGF-β1. We discovered that 1α,25(OH)(2)D(3) increased the expression of epithelial marker E-cadherin and decreased the level of mesenchymal marker, Vimentin, which was associated with the elevated expression of VDR. Moreover, 1α,25(OH)(2)D(3) reduced the expression level of transcription factors of EMT, such as slug, snail, and β-catenin. These results indicate that 1α,25(OH)(2)D(3) suppresses the migration and invasion of ovarian cancer cells by inhibiting EMT, implying that 1α,25(OH)(2)D(3) might be a potential therapeutic agent for the treatment of ovarian cancer. |
format | Online Article Text |
id | pubmed-5000682 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-50006822016-09-01 1α,25(OH)(2)D(3) Suppresses the Migration of Ovarian Cancer SKOV-3 Cells through the Inhibition of Epithelial–Mesenchymal Transition Hou, Yong-Feng Gao, Si-Hai Wang, Ping Zhang, He-Mei Liu, Li-Zhi Ye, Meng-Xuan Zhou, Guang-Ming Zhang, Zeng-Li Li, Bing-Yan Int J Mol Sci Article Ovarian cancer is the most lethal gynecological malignancy due to its high metastatic ability. Epithelial-mesenchymal transition (EMT) is essential during both follicular rupture and epithelium regeneration. However, it may also accelerate the progression of ovarian carcinomas. Experimental studies have found that 1α,25-dihydroxyvitamin-D3 [1α,25(OH)(2)D(3)] can inhibit the proliferation of ovarian cancer cells. In this study, we investigated whether 1α,25(OH)(2)D(3) could inhibit the migration of ovarian cancer cells via regulating EMT. We established a model of transient transforming growth factor-β1(TGF-β1)-induced EMT in human ovarian adenocarcinoma cell line SKOV-3 cells. Results showed that, compared with control, 1α,25(OH)(2)D(3) not only inhibited the migration and the invasion of SKOV-3 cells, but also promoted the acquisition of an epithelial phenotype of SKOV-3 cells treated with TGF-β1. We discovered that 1α,25(OH)(2)D(3) increased the expression of epithelial marker E-cadherin and decreased the level of mesenchymal marker, Vimentin, which was associated with the elevated expression of VDR. Moreover, 1α,25(OH)(2)D(3) reduced the expression level of transcription factors of EMT, such as slug, snail, and β-catenin. These results indicate that 1α,25(OH)(2)D(3) suppresses the migration and invasion of ovarian cancer cells by inhibiting EMT, implying that 1α,25(OH)(2)D(3) might be a potential therapeutic agent for the treatment of ovarian cancer. MDPI 2016-08-19 /pmc/articles/PMC5000682/ /pubmed/27548154 http://dx.doi.org/10.3390/ijms17081285 Text en © 2016 by the authors; licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC-BY) license (http://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Article Hou, Yong-Feng Gao, Si-Hai Wang, Ping Zhang, He-Mei Liu, Li-Zhi Ye, Meng-Xuan Zhou, Guang-Ming Zhang, Zeng-Li Li, Bing-Yan 1α,25(OH)(2)D(3) Suppresses the Migration of Ovarian Cancer SKOV-3 Cells through the Inhibition of Epithelial–Mesenchymal Transition |
title | 1α,25(OH)(2)D(3) Suppresses the Migration of Ovarian Cancer SKOV-3 Cells through the Inhibition of Epithelial–Mesenchymal Transition |
title_full | 1α,25(OH)(2)D(3) Suppresses the Migration of Ovarian Cancer SKOV-3 Cells through the Inhibition of Epithelial–Mesenchymal Transition |
title_fullStr | 1α,25(OH)(2)D(3) Suppresses the Migration of Ovarian Cancer SKOV-3 Cells through the Inhibition of Epithelial–Mesenchymal Transition |
title_full_unstemmed | 1α,25(OH)(2)D(3) Suppresses the Migration of Ovarian Cancer SKOV-3 Cells through the Inhibition of Epithelial–Mesenchymal Transition |
title_short | 1α,25(OH)(2)D(3) Suppresses the Migration of Ovarian Cancer SKOV-3 Cells through the Inhibition of Epithelial–Mesenchymal Transition |
title_sort | 1α,25(oh)(2)d(3) suppresses the migration of ovarian cancer skov-3 cells through the inhibition of epithelial–mesenchymal transition |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5000682/ https://www.ncbi.nlm.nih.gov/pubmed/27548154 http://dx.doi.org/10.3390/ijms17081285 |
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