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WTX inhibits gastric cancer migration through the reversal of epithelial-mesenchymal transition

The aim of the present study was to investigate whether the expression of Wilms' tumor gene on X chromosome (WTX) affected the epithelial-mesenchymal transition (EMT) process and migration of gastric cancer cells. Stable WTX-overexpressing AGS cells (AGS.W) were established and analyzed by flow...

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Autores principales: Ye, Danli, Ma, Wenxia, Xu, Jiahui, Zhu, Guifang, Liu, Deying, Liu, Chun, Ding, Yanqing, Zhang, Qingling
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6144879/
https://www.ncbi.nlm.nih.gov/pubmed/30250562
http://dx.doi.org/10.3892/ol.2018.9309
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author Ye, Danli
Ma, Wenxia
Xu, Jiahui
Zhu, Guifang
Liu, Deying
Liu, Chun
Ding, Yanqing
Zhang, Qingling
author_facet Ye, Danli
Ma, Wenxia
Xu, Jiahui
Zhu, Guifang
Liu, Deying
Liu, Chun
Ding, Yanqing
Zhang, Qingling
author_sort Ye, Danli
collection PubMed
description The aim of the present study was to investigate whether the expression of Wilms' tumor gene on X chromosome (WTX) affected the epithelial-mesenchymal transition (EMT) process and migration of gastric cancer cells. Stable WTX-overexpressing AGS cells (AGS.W) were established and analyzed by flow cytometry. The efficiency of the overexpression was verified by fluorescence microscopy, reverse transcription-quantitative polymerase chain reaction and western blotting. To analyze the expression of EMT-associated proteins, western blotting and immunofluorescence assays were performed. The migratory capability of the cells was detected by Transwell wound-healing assays, respectively. Compared with that of the control cells (AGS.veh), WTX expression was notably increased at mRNA (P<0.05) and protein levels (P<0.05) in the AGS.W gastric cancer cells. Morphological observations indicated that AGS.W cells transformed into spindle shapes, compared to AGS.veh cells, which maintained round or oval shapes. Furthermore, western blotting and immunofluorescence validated that the expression level of the epithelial marker epithelial-cadherin was significantly increased, whereas the expression levels of the mesenchymal markers neural-cadherin, β-catenin and vimentin were significantly decreased in the AGS.W cells compared with those in the AGS.veh cells. In addition, the overexpression of WTX decreased the migratory ability of AGS.W cells compared with AGS.veh cells. Exogenous expression of WTX inhibited gastric cancer cell migration by reversing EMT. The results of the present study describe a molecular feature that may be a promising target for future gastric cancer therapy strategies.
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spelling pubmed-61448792018-09-24 WTX inhibits gastric cancer migration through the reversal of epithelial-mesenchymal transition Ye, Danli Ma, Wenxia Xu, Jiahui Zhu, Guifang Liu, Deying Liu, Chun Ding, Yanqing Zhang, Qingling Oncol Lett Articles The aim of the present study was to investigate whether the expression of Wilms' tumor gene on X chromosome (WTX) affected the epithelial-mesenchymal transition (EMT) process and migration of gastric cancer cells. Stable WTX-overexpressing AGS cells (AGS.W) were established and analyzed by flow cytometry. The efficiency of the overexpression was verified by fluorescence microscopy, reverse transcription-quantitative polymerase chain reaction and western blotting. To analyze the expression of EMT-associated proteins, western blotting and immunofluorescence assays were performed. The migratory capability of the cells was detected by Transwell wound-healing assays, respectively. Compared with that of the control cells (AGS.veh), WTX expression was notably increased at mRNA (P<0.05) and protein levels (P<0.05) in the AGS.W gastric cancer cells. Morphological observations indicated that AGS.W cells transformed into spindle shapes, compared to AGS.veh cells, which maintained round or oval shapes. Furthermore, western blotting and immunofluorescence validated that the expression level of the epithelial marker epithelial-cadherin was significantly increased, whereas the expression levels of the mesenchymal markers neural-cadherin, β-catenin and vimentin were significantly decreased in the AGS.W cells compared with those in the AGS.veh cells. In addition, the overexpression of WTX decreased the migratory ability of AGS.W cells compared with AGS.veh cells. Exogenous expression of WTX inhibited gastric cancer cell migration by reversing EMT. The results of the present study describe a molecular feature that may be a promising target for future gastric cancer therapy strategies. D.A. Spandidos 2018-10 2018-08-16 /pmc/articles/PMC6144879/ /pubmed/30250562 http://dx.doi.org/10.3892/ol.2018.9309 Text en Copyright: © Ye 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
Ye, Danli
Ma, Wenxia
Xu, Jiahui
Zhu, Guifang
Liu, Deying
Liu, Chun
Ding, Yanqing
Zhang, Qingling
WTX inhibits gastric cancer migration through the reversal of epithelial-mesenchymal transition
title WTX inhibits gastric cancer migration through the reversal of epithelial-mesenchymal transition
title_full WTX inhibits gastric cancer migration through the reversal of epithelial-mesenchymal transition
title_fullStr WTX inhibits gastric cancer migration through the reversal of epithelial-mesenchymal transition
title_full_unstemmed WTX inhibits gastric cancer migration through the reversal of epithelial-mesenchymal transition
title_short WTX inhibits gastric cancer migration through the reversal of epithelial-mesenchymal transition
title_sort wtx inhibits gastric cancer migration through the reversal of epithelial-mesenchymal transition
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6144879/
https://www.ncbi.nlm.nih.gov/pubmed/30250562
http://dx.doi.org/10.3892/ol.2018.9309
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