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The transcription factor ZEB1 promotes an aggressive phenotype in prostate cancer cell lines

The transcription factor ZEB1 promotes an aggressive phenotype in prostate cancer cell lines

作     者:Octavio Orellana-Serradell Daniela Herrera Enrique A Castellon Hector R Contreras 

作者机构:Department of Basic and Clinical Oncology Faculty of Medicine University of Chile Independencia Santiago 8380453 Chile. 

出 版 物:《Asian Journal of Andrology》 (亚洲男性学杂志(英文版))

年 卷 期:2018年第20卷第3期

页      面:294-299页

核心收录:

学科分类:0710[理学-生物学] 080705[工学-制冷及低温工程] 1002[医学-临床医学] 07[理学] 08[工学] 0807[工学-动力工程及工程热物理] 071002[理学-动物学] 

基  金:the Fondo Nacional de Ciencia y Tecnologia (FONDECYT Comision Nacional de Investigacion Cientifica y Tecnologica (CONICYT 

主  题:epithelial-mesenchymal transition prostate cancer transcriptional repression ZEB1 

摘      要:It has been reported that one of the factors that promotes tumoral progression is the abnormal activation of the epithelial-mesenchymal transition program. This process is associated with tumoral cells acquiring invasive and malignant properties and has the transcription factor zinc finger E-box-binding homeobox 1 (ZEB1) as one of its main activators. However, the role of ZEB1 in promoting malignancy in prostate cancer (PC, a) is still unclear. Here, we report that ZEB1 expression correlates with Gleason score in PCa samples and that expression of ZEB1 regulates epithelial-mesenchymal transition and malignant characteristics in PCa cell lines. The results showed that ZEB1 expression is higher in samples of higher malignancy and that overexpression of ZEB1 was able to induce epithelial-mesenchymal transition by upregulating the mesenchymal marker Vimentin and downregulating the epithelial marker E-Cadherin. On the contrary, ZEB 1 silencing repressed Vimentin expression and upregulated E-Cadherin. ZEB1 expression conferred enhanced motility and invasiveness and a higher colony formation capacity to 22Rvl cells whereas DU145 cells with ZEB1 silencing showed a decrease in those same properties. The results showed that ZEB1 could be a key promoter of tumoral progression toward advanced stages of PC, a.

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