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Conference Paper: Id-1 promotes TGF-β1-induced cell motility through MEK-ERK-mediated HSP27 activation in prostate epithelial cells

TitleId-1 promotes TGF-β1-induced cell motility through MEK-ERK-mediated HSP27 activation in prostate epithelial cells
Authors
Issue Date2007
PublisherAmerican Association for Cancer Research.
Citation
The 98th Annual Meeting of the American Association for Cancer Research (AACR 2007), Los Angeles, CA., 14-18 April 2007. In Cancer Research, 2007, v. 67 n. 9S, p. 4939 How to Cite?
AbstractId-1 (inhibitor of differentiation or DNA binding-1) gene encodes a helix-loop helix protein which dimerizes and blocks the basic HLH protein from binding DNA. It 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 transforming growth factor β1 (TGF-β1). Here we demonstrate a critical role of Id-1 in promoting TGF-β1-induced cell motility in a non-malignant prostate epithelial cell line, NPTX cells. We found that ectopic Id-1 expression promoted F-actin stress fiber formation which was associated with increased cell-substrate adhesion, in TGF-β1-treated cells. This process was mediated through activation of MEK-ERK signaling pathway and subsequent activation of heat shock protein 27 (Hsp27). In addition, our results also indicated that Id-1 overexpression led to disruption of the adherens junction complex at cell-cell contacts through down-regulation of E-cadherin and redistribution of cellular localization of β-catenin, along with up-regulation of N-cadherin in the TGF-β1-treated cells. These lines of evidence reveal a novel tumor promoting 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. [Supported by RGC grants (HKU7478/03M) to XHW and YCW (HKU7490.03M, 7470/04M, NSFC/RGC N_HKU738/03, HKU Foundation Seed Fund, 03)].
Persistent Identifierhttp://hdl.handle.net/10722/95233
ISSN
2015 Impact Factor: 8.556
2015 SCImago Journal Rankings: 5.372

 

DC FieldValueLanguage
dc.contributor.authorWong, YCen_HK
dc.contributor.authorDi, Ken_HK
dc.contributor.authorLing, MTen_HK
dc.contributor.authorWang, Xen_HK
dc.date.accessioned2010-09-25T15:55:48Z-
dc.date.available2010-09-25T15:55:48Z-
dc.date.issued2007en_HK
dc.identifier.citationThe 98th Annual Meeting of the American Association for Cancer Research (AACR 2007), Los Angeles, CA., 14-18 April 2007. In Cancer Research, 2007, v. 67 n. 9S, p. 4939en_HK
dc.identifier.issn0008-5472-
dc.identifier.urihttp://hdl.handle.net/10722/95233-
dc.description.abstractId-1 (inhibitor of differentiation or DNA binding-1) gene encodes a helix-loop helix protein which dimerizes and blocks the basic HLH protein from binding DNA. It 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 transforming growth factor β1 (TGF-β1). Here we demonstrate a critical role of Id-1 in promoting TGF-β1-induced cell motility in a non-malignant prostate epithelial cell line, NPTX cells. We found that ectopic Id-1 expression promoted F-actin stress fiber formation which was associated with increased cell-substrate adhesion, in TGF-β1-treated cells. This process was mediated through activation of MEK-ERK signaling pathway and subsequent activation of heat shock protein 27 (Hsp27). In addition, our results also indicated that Id-1 overexpression led to disruption of the adherens junction complex at cell-cell contacts through down-regulation of E-cadherin and redistribution of cellular localization of β-catenin, along with up-regulation of N-cadherin in the TGF-β1-treated cells. These lines of evidence reveal a novel tumor promoting 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. [Supported by RGC grants (HKU7478/03M) to XHW and YCW (HKU7490.03M, 7470/04M, NSFC/RGC N_HKU738/03, HKU Foundation Seed Fund, 03)].-
dc.languageengen_HK
dc.publisherAmerican Association for Cancer Research.-
dc.relation.ispartofCancer Researchen_HK
dc.titleId-1 promotes TGF-β1-induced cell motility through MEK-ERK-mediated HSP27 activation in prostate epithelial cellsen_HK
dc.typeConference_Paperen_HK
dc.identifier.emailWong, YC: ycwong@hkucc.hku.hken_HK
dc.identifier.emailLing, MT: patling@HKUCC.hku.hken_HK
dc.identifier.authorityWong, YC=rp00316en_HK
dc.identifier.authorityLing, MT=rp00449en_HK
dc.identifier.hkuros147357en_HK
dc.identifier.volume67-
dc.identifier.issue9S-
dc.identifier.spage4939-
dc.identifier.epage4939-

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