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Article: Id-1 promotes TGF-β1-induced cell motility through HSP27 activation and disassembly of adherens junction in prostate epithelial cells

TitleId-1 promotes TGF-β1-induced cell motility through HSP27 activation and disassembly of adherens junction in prostate epithelial cells
Authors
Issue Date2007
PublisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/locate/yexcr
Citation
Experimental Cell Research, 2007, v. 313 n. 19, p. 3983-3999 How to Cite?
AbstractId-1 (inhibitor of differentiation or DNA binding-1) has been positively associated with cell proliferation, cell cycle progression, and invasiveness during tumorigenesis. In addition, Id-1 has been shown to modulate cellular sensitivity to TGF-β1 (transforming growth factor β1). Here we demonstrate a novel role of Id-1 in promoting TGF-β1-induced cell motility in a non-malignant prostate epithelial cell line, NPTX. We found that Id-1 promoted F-actin stress fiber formation in response to TGF-β1, which was associated with increased cell-substrate adhesion and cell migration in NPTX cells. In addition, this positive effect of Id-1 on TGF-β1-induced cell motility was mediated through activation of MEK-ERK signaling pathway and subsequent phosphorylation of HSP27 (heat shock protein 27). Furthermore, Id-1 disrupted the adherens junction complex in TGF-β1-treated cells through down-regulation of E-cadherin, redistribution of β-catenin, along with up-regulation of N-cadherin. These lines of evidence reveal a novel tumorigenic role of Id-1 through reorganization of actin cytoskeleton and disassembly of cell-cell adhesion in response to TGF-β1 in human prostate epithelial cells, and suggest that intracellular Id-1 levels might be a determining factor for switching TGF-β1 from a growth inhibitor to a tumor promoter during prostate carcinogenesis. © 2007 Elsevier Inc. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/149676
ISSN
2015 Impact Factor: 3.378
2015 SCImago Journal Rankings: 1.900
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorDi, Ken_US
dc.contributor.authorWong, YCen_US
dc.contributor.authorWang, Xen_US
dc.date.accessioned2012-06-26T05:56:57Z-
dc.date.available2012-06-26T05:56:57Z-
dc.date.issued2007en_US
dc.identifier.citationExperimental Cell Research, 2007, v. 313 n. 19, p. 3983-3999en_US
dc.identifier.issn0014-4827en_US
dc.identifier.urihttp://hdl.handle.net/10722/149676-
dc.description.abstractId-1 (inhibitor of differentiation or DNA binding-1) has been positively associated with cell proliferation, cell cycle progression, and invasiveness during tumorigenesis. In addition, Id-1 has been shown to modulate cellular sensitivity to TGF-β1 (transforming growth factor β1). Here we demonstrate a novel role of Id-1 in promoting TGF-β1-induced cell motility in a non-malignant prostate epithelial cell line, NPTX. We found that Id-1 promoted F-actin stress fiber formation in response to TGF-β1, which was associated with increased cell-substrate adhesion and cell migration in NPTX cells. In addition, this positive effect of Id-1 on TGF-β1-induced cell motility was mediated through activation of MEK-ERK signaling pathway and subsequent phosphorylation of HSP27 (heat shock protein 27). Furthermore, Id-1 disrupted the adherens junction complex in TGF-β1-treated cells through down-regulation of E-cadherin, redistribution of β-catenin, along with up-regulation of N-cadherin. These lines of evidence reveal a novel tumorigenic role of Id-1 through reorganization of actin cytoskeleton and disassembly of cell-cell adhesion in response to TGF-β1 in human prostate epithelial cells, and suggest that intracellular Id-1 levels might be a determining factor for switching TGF-β1 from a growth inhibitor to a tumor promoter during prostate carcinogenesis. © 2007 Elsevier Inc. All rights reserved.en_US
dc.languageengen_US
dc.publisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/locate/yexcren_US
dc.relation.ispartofExperimental Cell Researchen_US
dc.subject.meshAdherens Junctions - Ultrastructureen_US
dc.subject.meshCadherins - Genetics - Metabolismen_US
dc.subject.meshCell Lineen_US
dc.subject.meshCell Movementen_US
dc.subject.meshEpithelial Cells - Cytologyen_US
dc.subject.meshHsp27 Heat-Shock Proteinsen_US
dc.subject.meshHeat-Shock Proteins - Metabolismen_US
dc.subject.meshHumansen_US
dc.subject.meshInhibitor Of Differentiation Protein 1 - Genetics - Pharmacologyen_US
dc.subject.meshMap Kinase Signaling Systemen_US
dc.subject.meshMaleen_US
dc.subject.meshNeoplasm Proteins - Metabolismen_US
dc.subject.meshProstate - Cytologyen_US
dc.subject.meshStress Fibersen_US
dc.subject.meshTransforming Growth Factor Beta1 - Physiologyen_US
dc.titleId-1 promotes TGF-β1-induced cell motility through HSP27 activation and disassembly of adherens junction in prostate epithelial cellsen_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.yexcr.2007.08.023en_US
dc.identifier.pmid17916352-
dc.identifier.scopuseid_2-s2.0-35448988159en_US
dc.identifier.hkuros138887-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-35448988159&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume313en_US
dc.identifier.issue19en_US
dc.identifier.spage3983en_US
dc.identifier.epage3999en_US
dc.identifier.isiWOS:000250769600004-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridDi, K=14526710900en_US
dc.identifier.scopusauthoridWong, YC=7403041798en_US
dc.identifier.scopusauthoridWang, X=7501854829en_US

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