Article: A novel role of Id-1 in regulation of epithelial-to-mesenchymal transition in bladder cancer

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Publisher Website: 10.1016/j.urolonc.2011.12.003
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Title	A novel role of Id-1 in regulation of epithelial-to-mesenchymal transition in bladder cancer
Authors	Hu, H3 Wang, YL3 Wang, GW3 Wong, YC2 Wang, XF3 Wang, Y1 Xu, KX3
Keywords	Bladder Cancer Epithelial-To-Mesenchymal Transition Id-1
Issue Date	2012
Publisher	Elsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/urolonco
Citation	Urologic Oncology: Seminars And Original Investigations, 2012 [How to Cite?] DOI: http://dx.doi.org/10.1016/j.urolonc.2011.12.003
Abstract	Background and objective: Inhibitor of differentiation or DNA binding -1 (Id-1) has been shown to be increased in several types of advanced cancer, and to be associated with aggressive and metastatic abilities of cancer cells. Recently, more and more evidence indicates that epithelial-to-mesenchymal transition (EMT) is an important mechanism taking place during tumor invasion and metastasis, but the molecular pathways underlying EMT have not been clearly established. This study was to investigate the expression of Id-1 in bladder cancer and its association with EMT. Materials and methods: A total of 169 tissues, consisting of 147 primary bladder cancers and 22 adjacent normal tissues were included in this study. Id-1, E-cadherin, and β-catenin were examined immunohistochemically in paraffin sections. The pBabe-Id-1 expression retroviral vector and retroviral vectors containing an Id-1-specific small interfering RNA oligonucleotides (si-Id-1) were transfected into 2 bladder cancer cell lines respectively. Then, we used Western blotting and immunofluorescent staining to detect the cellular expression of epithelial markers and mesenchymal markers. The invasion and migration ability of bladder cancer cells were identified by type I collagen invasion assay and wound closure assay. Results: We demonstrated that increased Id-1 expression was associated with advanced tumor stage and grade. In addition, the increased Id-1 expression in bladder tumors was also correlated with decreased membranous E-cadherin and β-catenin expression. In vitro, studies showed that inactivation of the Id-1 gene conferred morphologic transition of bladder cancer cells from a fibroblastic to epithelial appearance, and overexpression of Id-1 could lead to acquisition of a fibroblastic spindle cell phenotype accompanied by loss of cell-to-cell contacts. By Western blotting and immunofluorescent staining, we showed that the expression level of Id-1 was correlated with the expression of mesenchymal markers but was inversely correlated with the expression of epithelial markers. Moreover, results of collagen invasion and wound closure assays showed ectopic Id-1 expression led to increased ability of invasion and migration. Conclusions: Our results suggest that Id-1 may play roles in tumor progression and EMT activation in bladder cancer. © 2011 Elsevier Inc. All rights reserved.
ISSN	1078-1439 2011 Impact Factor: 3.216 2011 SCImago Journal Rankings: 0.259
DOI	http://dx.doi.org/10.1016/j.urolonc.2011.12.003

DC Field	Value
dc.contributor.author	Hu, H
dc.contributor.author	Wang, YL
dc.contributor.author	Wang, GW
dc.contributor.author	Wong, YC
dc.contributor.author	Wang, XF
dc.contributor.author	Wang, Y
dc.contributor.author	Xu, KX
dc.date.accessioned	2012-06-26T05:58:26Z
dc.date.available	2012-06-26T05:58:26Z
dc.date.issued	2012
dc.description.abstract	Background and objective: Inhibitor of differentiation or DNA binding -1 (Id-1) has been shown to be increased in several types of advanced cancer, and to be associated with aggressive and metastatic abilities of cancer cells. Recently, more and more evidence indicates that epithelial-to-mesenchymal transition (EMT) is an important mechanism taking place during tumor invasion and metastasis, but the molecular pathways underlying EMT have not been clearly established. This study was to investigate the expression of Id-1 in bladder cancer and its association with EMT. Materials and methods: A total of 169 tissues, consisting of 147 primary bladder cancers and 22 adjacent normal tissues were included in this study. Id-1, E-cadherin, and β-catenin were examined immunohistochemically in paraffin sections. The pBabe-Id-1 expression retroviral vector and retroviral vectors containing an Id-1-specific small interfering RNA oligonucleotides (si-Id-1) were transfected into 2 bladder cancer cell lines respectively. Then, we used Western blotting and immunofluorescent staining to detect the cellular expression of epithelial markers and mesenchymal markers. The invasion and migration ability of bladder cancer cells were identified by type I collagen invasion assay and wound closure assay. Results: We demonstrated that increased Id-1 expression was associated with advanced tumor stage and grade. In addition, the increased Id-1 expression in bladder tumors was also correlated with decreased membranous E-cadherin and β-catenin expression. In vitro, studies showed that inactivation of the Id-1 gene conferred morphologic transition of bladder cancer cells from a fibroblastic to epithelial appearance, and overexpression of Id-1 could lead to acquisition of a fibroblastic spindle cell phenotype accompanied by loss of cell-to-cell contacts. By Western blotting and immunofluorescent staining, we showed that the expression level of Id-1 was correlated with the expression of mesenchymal markers but was inversely correlated with the expression of epithelial markers. Moreover, results of collagen invasion and wound closure assays showed ectopic Id-1 expression led to increased ability of invasion and migration. Conclusions: Our results suggest that Id-1 may play roles in tumor progression and EMT activation in bladder cancer. © 2011 Elsevier Inc. All rights reserved.
dc.description.nature	Link_to_subscribed_fulltext
dc.identifier.citation	Urologic Oncology: Seminars And Original Investigations, 2012 [How to Cite?] DOI: http://dx.doi.org/10.1016/j.urolonc.2011.12.003
dc.identifier.citeulike	10235213
dc.identifier.doi	http://dx.doi.org/10.1016/j.urolonc.2011.12.003
dc.identifier.issn	1078-1439 2011 Impact Factor: 3.216 2011 SCImago Journal Rankings: 0.259
dc.identifier.scopus	eid_2-s2.0-84855287916
dc.identifier.uri	http://hdl.handle.net/10722/149775
dc.language	eng
dc.publisher	Elsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/urolonco
dc.publisher.place	United States
dc.relation.ispartof	Urologic Oncology: Seminars and Original Investigations
dc.subject	Bladder Cancer
dc.subject	Epithelial-To-Mesenchymal Transition
dc.subject	Id-1
dc.title	A novel role of Id-1 in regulation of epithelial-to-mesenchymal transition in bladder cancer
dc.type	Article

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Author Affiliations

Peking University Health Science Center
The University of Hong Kong
Peking University

Article: A novel role of Id-1 in regulation of epithelial-to-mesenchymal transition in bladder cancer

The HKU Scholars Hub has contact details for these author(s).