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Article: Transforming growth factor-β1 attenuates junctional adhesion molecule-A and contributes to breast cancer cell invasion

TitleTransforming growth factor-β1 attenuates junctional adhesion molecule-A and contributes to breast cancer cell invasion
Authors
KeywordsInvasion
JAM-A
TGF-β1
Issue Date2012
PublisherPergamon. The Journal's web site is located at http://www.elsevier.com/locate/ejca
Citation
European Journal of Cancer, 2012, v. 48 n. 18, p. 3475-3487 How to Cite?
AbstractTransforming growth factor-beta1 (TGF-beta1) is a potent regulator in promoting the invasion and proliferation of breast cancer cells. Junctional adhesion molecule-A (JAM-A) is a tight junction protein that displays an inverse relationship to cell invasiveness in breast cancer cells. Whether TGF-beta1 signaling induces alteration of JAM-A expression leading to cell invasion has not been investigated. In this study, we report that TGF-beta1 down-regulated JAM-A expression via its effect on both transcriptional and post-translational regulations of JAM-A, thus inducing cell invasion. On exploring whether TGF-beta1 might be the upstream regulator of JAM-A expression, we found that knockdown of TGF-beta receptors and canonical Smad signaling could upregulate JAM-A level and inhibit cell invasion in MDA-MB-231 cells. TGF-beta1 treatment of MCF-7 cells caused a significant reduction of JAM-A mRNA and protein and induced cell invasion. Delineating the signal mechanisms involved in TGF-beta1-mediated JAM-A repression, we found that TGF-beta1 significantly inhibited JAM-A gene transcription via the activation of Smads. In addition to Smad activation, we found that involvement of p54 JNK is crucial for post-translational modification of TGF-beta1-mediated JAM-A protein degradation. Blockage of JNK pathway by inhibitor could attenuate TGF-beta1-induced cell invasion. We provide evidences for the first time that TGF-beta1 induces breast cancer cell invasion via TGF-beta1-mediated control on JAM-A expression. Identification of JAM-A as a downstream target of TGF-beta1 represents a crucial mechanism in cancer progression.
Persistent Identifierhttp://hdl.handle.net/10722/165939
ISSN
2015 Impact Factor: 6.163
2015 SCImago Journal Rankings: 3.152
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorWang, Yen_HK
dc.contributor.authorLui, WYen_HK
dc.date.accessioned2012-09-20T08:25:41Z-
dc.date.available2012-09-20T08:25:41Z-
dc.date.issued2012en_HK
dc.identifier.citationEuropean Journal of Cancer, 2012, v. 48 n. 18, p. 3475-3487en_HK
dc.identifier.issn0959-8049en_HK
dc.identifier.urihttp://hdl.handle.net/10722/165939-
dc.description.abstractTransforming growth factor-beta1 (TGF-beta1) is a potent regulator in promoting the invasion and proliferation of breast cancer cells. Junctional adhesion molecule-A (JAM-A) is a tight junction protein that displays an inverse relationship to cell invasiveness in breast cancer cells. Whether TGF-beta1 signaling induces alteration of JAM-A expression leading to cell invasion has not been investigated. In this study, we report that TGF-beta1 down-regulated JAM-A expression via its effect on both transcriptional and post-translational regulations of JAM-A, thus inducing cell invasion. On exploring whether TGF-beta1 might be the upstream regulator of JAM-A expression, we found that knockdown of TGF-beta receptors and canonical Smad signaling could upregulate JAM-A level and inhibit cell invasion in MDA-MB-231 cells. TGF-beta1 treatment of MCF-7 cells caused a significant reduction of JAM-A mRNA and protein and induced cell invasion. Delineating the signal mechanisms involved in TGF-beta1-mediated JAM-A repression, we found that TGF-beta1 significantly inhibited JAM-A gene transcription via the activation of Smads. In addition to Smad activation, we found that involvement of p54 JNK is crucial for post-translational modification of TGF-beta1-mediated JAM-A protein degradation. Blockage of JNK pathway by inhibitor could attenuate TGF-beta1-induced cell invasion. We provide evidences for the first time that TGF-beta1 induces breast cancer cell invasion via TGF-beta1-mediated control on JAM-A expression. Identification of JAM-A as a downstream target of TGF-beta1 represents a crucial mechanism in cancer progression.en_HK
dc.languageengen_US
dc.publisherPergamon. The Journal's web site is located at http://www.elsevier.com/locate/ejcaen_HK
dc.relation.ispartofEuropean Journal of Canceren_HK
dc.subjectInvasionen_HK
dc.subjectJAM-Aen_HK
dc.subjectTGF-β1en_HK
dc.titleTransforming growth factor-β1 attenuates junctional adhesion molecule-A and contributes to breast cancer cell invasionen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0959-8049&volume=&spage=&epage=&date=2012&atitle=Transforming+growth+factor-β1+attenuates+junctional+adhesion+molecule-A+and+contributes+to+breast+cancer+cell+invasionen_US
dc.identifier.emailWang, Y: wyang@hkucc.hku.hken_HK
dc.identifier.emailLui, WY: wylui@hku.hk-
dc.identifier.authorityLui, WY=rp00756en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.ejca.2012.04.016en_HK
dc.identifier.pmid22647687-
dc.identifier.scopuseid_2-s2.0-84869502116en_HK
dc.identifier.hkuros206216en_US
dc.identifier.volume48-
dc.identifier.issue18-
dc.identifier.spage3475-
dc.identifier.epage3487-
dc.identifier.eissn1879-0852-
dc.identifier.isiWOS:000311218100017-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridLui, WY=35220192400en_HK
dc.identifier.scopusauthoridWang, Y=7601513691en_HK
dc.identifier.citeulike10726906-

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