File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

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

TitleA novel role of Id-1 in regulation of epithelial-to-mesenchymal transition in bladder cancer
Authors
KeywordsBladder Cancer
Epithelial-To-Mesenchymal Transition
Id-1
Issue Date2013
PublisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/urolonco
Citation
Urologic Oncology: Seminars And Original Investigations, 2013, v. 31 n. 7, p. 1242-1253 How to Cite?
AbstractBackground 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.
Persistent Identifierhttp://hdl.handle.net/10722/149775
ISSN
2023 Impact Factor: 2.4
2023 SCImago Journal Rankings: 0.867
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorHu, Hen_US
dc.contributor.authorWang, YLen_US
dc.contributor.authorWang, GWen_US
dc.contributor.authorWong, YCen_US
dc.contributor.authorWang, XFen_US
dc.contributor.authorWang, Yen_US
dc.contributor.authorXu, KXen_US
dc.date.accessioned2012-06-26T05:58:26Z-
dc.date.available2012-06-26T05:58:26Z-
dc.date.issued2013en_US
dc.identifier.citationUrologic Oncology: Seminars And Original Investigations, 2013, v. 31 n. 7, p. 1242-1253en_US
dc.identifier.issn1078-1439en_US
dc.identifier.urihttp://hdl.handle.net/10722/149775-
dc.description.abstractBackground 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.en_US
dc.languageengen_US
dc.publisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/uroloncoen_US
dc.relation.ispartofUrologic Oncology: Seminars and Original Investigationsen_US
dc.subjectBladder Canceren_US
dc.subjectEpithelial-To-Mesenchymal Transitionen_US
dc.subjectId-1en_US
dc.titleA novel role of Id-1 in regulation of epithelial-to-mesenchymal transition in bladder canceren_US
dc.typeArticleen_US
dc.identifier.emailWong, YC:ycwong@hkucc.hku.hken_US
dc.identifier.authorityWong, YC=rp00316en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1016/j.urolonc.2011.12.003en_US
dc.identifier.pmid22226665-
dc.identifier.scopuseid_2-s2.0-84884672985en_US
dc.identifier.isiWOS:000325664300041-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridHu, H=36812244900en_US
dc.identifier.scopusauthoridWang, YL=47461691100en_US
dc.identifier.scopusauthoridWang, GW=23502085700en_US
dc.identifier.scopusauthoridWong, YC=7403041798en_US
dc.identifier.scopusauthoridWang, XF=34873964600en_US
dc.identifier.scopusauthoridWang, Y=54881287300en_US
dc.identifier.scopusauthoridXu, KX=7403282051en_US
dc.identifier.citeulike10235213-
dc.identifier.issnl1078-1439-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats