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Article: Adhesion-independent mechanism for suppression of tumor cell invasion by E-cadherin

TitleAdhesion-independent mechanism for suppression of tumor cell invasion by E-cadherin
Authors
KeywordsAdhesion
B-catenin
E-cadherin
Invasion
Signaling
Issue Date2003
PublisherRockefeller University Press. The Journal's web site is located at http://www.jcb.org
Citation
Journal Of Cell Biology, 2003, v. 161 n. 6, p. 1191-1203 How to Cite?
AbstractLoss of E-cadherin expression or function in tumors leads to a more invasive phenotype. In this study, we investigated whether the invasion suppressor activity of E-cadherin is mediated directly by tighter physical cell adhesion, indirectly by sequestering β-catenin and thus antagonizing β-catenin/T cell factor (TCF) signaling, or by other signaling pathways. To distinguish mechanisms, we expressed wild-type E-cadherin and various E-cadherin mutants in invasive E-cadherin-negative human breast (MDA-MB-231) and prostate (TSU-Pr1) epithelial carcinoma cell lines using a tetracycline-inducible system. Our data confirm that E-cadherin inhibits human mammary and prostate tumor cell invasion. We find that adhesion is neither necessary nor sufficient for suppressing cancer invasion. Rather, the invasion suppressor signal is mediated through the β-catenin-binding domain of the E-cadherin cytoplasmic tail but not through the p120 ctn-binding domain. β-catenin depletion also results in invasion suppression. However, alteration in the β-catenin/TCF transcriptional regulation of target genes is not required for the invasion suppressor activity of E-cadherin, suggesting the involvement of other β-catenin-binding proteins.
Persistent Identifierhttp://hdl.handle.net/10722/42267
ISSN
2015 Impact Factor: 8.717
2015 SCImago Journal Rankings: 7.923
PubMed Central ID
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorWong, ASTen_HK
dc.contributor.authorGumbiner, BMen_HK
dc.date.accessioned2007-01-08T02:33:04Z-
dc.date.available2007-01-08T02:33:04Z-
dc.date.issued2003en_HK
dc.identifier.citationJournal Of Cell Biology, 2003, v. 161 n. 6, p. 1191-1203en_HK
dc.identifier.issn0021-9525en_HK
dc.identifier.urihttp://hdl.handle.net/10722/42267-
dc.description.abstractLoss of E-cadherin expression or function in tumors leads to a more invasive phenotype. In this study, we investigated whether the invasion suppressor activity of E-cadherin is mediated directly by tighter physical cell adhesion, indirectly by sequestering β-catenin and thus antagonizing β-catenin/T cell factor (TCF) signaling, or by other signaling pathways. To distinguish mechanisms, we expressed wild-type E-cadherin and various E-cadherin mutants in invasive E-cadherin-negative human breast (MDA-MB-231) and prostate (TSU-Pr1) epithelial carcinoma cell lines using a tetracycline-inducible system. Our data confirm that E-cadherin inhibits human mammary and prostate tumor cell invasion. We find that adhesion is neither necessary nor sufficient for suppressing cancer invasion. Rather, the invasion suppressor signal is mediated through the β-catenin-binding domain of the E-cadherin cytoplasmic tail but not through the p120 ctn-binding domain. β-catenin depletion also results in invasion suppression. However, alteration in the β-catenin/TCF transcriptional regulation of target genes is not required for the invasion suppressor activity of E-cadherin, suggesting the involvement of other β-catenin-binding proteins.en_HK
dc.format.extent583264 bytes-
dc.format.extent29696 bytes-
dc.format.mimetypeapplication/pdf-
dc.format.mimetypeapplication/msword-
dc.languageengen_HK
dc.publisherRockefeller University Press. The Journal's web site is located at http://www.jcb.orgen_HK
dc.relation.ispartofJournal of Cell Biologyen_HK
dc.rightsThe Journal of Cell Biology. Copyright © Rockefeller University Press.en_HK
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.subjectAdhesionen_HK
dc.subjectB-cateninen_HK
dc.subjectE-cadherinen_HK
dc.subjectInvasionen_HK
dc.subjectSignalingen_HK
dc.subject.meshCadherins - genetics - metabolismen_HK
dc.subject.meshCell adhesion - physiologyen_HK
dc.subject.meshCell membrane - metabolismen_HK
dc.subject.meshNeoplasm invasiveness - physiopathologyen_HK
dc.subject.meshNeoplasms - metabolism - physiopathologyen_HK
dc.titleAdhesion-independent mechanism for suppression of tumor cell invasion by E-cadherinen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0021-9525&volume=161&issue=6&spage=1191&epage=1203&date=2003&atitle=Adhesion-independent+mechanism+for+suppression+of+tumor+cell+invasion+by+E-cadherinen_HK
dc.identifier.emailWong, AST: awong1@hkucc.hku.hken_HK
dc.identifier.authorityWong, AST=rp00805en_HK
dc.description.naturepublished_or_final_versionen_HK
dc.identifier.doi10.1083/jcb.200212033en_HK
dc.identifier.pmid12810698-
dc.identifier.pmcidPMC2173007-
dc.identifier.scopuseid_2-s2.0-0037477627en_HK
dc.identifier.hkuros91125-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0037477627&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume161en_HK
dc.identifier.issue6en_HK
dc.identifier.spage1191en_HK
dc.identifier.epage1203en_HK
dc.identifier.isiWOS:000183827400018-
dc.publisher.placeUnited Statesen_HK
dc.identifier.f10001014212-
dc.identifier.scopusauthoridWong, AST=23987963300en_HK
dc.identifier.scopusauthoridGumbiner, BM=7005377389en_HK
dc.identifier.citeulike5297872-

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