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- Publisher Website: 10.1016/j.ejca.2012.04.016
- Scopus: eid_2-s2.0-84869502116
- PMID: 22647687
- WOS: WOS:000311218100017
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Article: Transforming growth factor-β1 attenuates junctional adhesion molecule-A and contributes to breast cancer cell invasion
Title | Transforming growth factor-β1 attenuates junctional adhesion molecule-A and contributes to breast cancer cell invasion |
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Authors | |
Keywords | Invasion JAM-A TGF-β1 |
Issue Date | 2012 |
Publisher | Pergamon. 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? |
Abstract | Transforming 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 Identifier | http://hdl.handle.net/10722/165939 |
ISSN | 2021 Impact Factor: 10.002 2020 SCImago Journal Rankings: 3.354 |
ISI Accession Number ID |
DC Field | Value | Language |
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dc.contributor.author | Wang, Y | en_HK |
dc.contributor.author | Lui, WY | en_HK |
dc.date.accessioned | 2012-09-20T08:25:41Z | - |
dc.date.available | 2012-09-20T08:25:41Z | - |
dc.date.issued | 2012 | en_HK |
dc.identifier.citation | European Journal of Cancer, 2012, v. 48 n. 18, p. 3475-3487 | en_HK |
dc.identifier.issn | 0959-8049 | en_HK |
dc.identifier.uri | http://hdl.handle.net/10722/165939 | - |
dc.description.abstract | Transforming 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.language | eng | en_US |
dc.publisher | Pergamon. The Journal's web site is located at http://www.elsevier.com/locate/ejca | en_HK |
dc.relation.ispartof | European Journal of Cancer | en_HK |
dc.subject | Invasion | en_HK |
dc.subject | JAM-A | en_HK |
dc.subject | TGF-β1 | en_HK |
dc.title | Transforming growth factor-β1 attenuates junctional adhesion molecule-A and contributes to breast cancer cell invasion | en_HK |
dc.type | Article | en_HK |
dc.identifier.openurl | http://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+invasion | en_US |
dc.identifier.email | Wang, Y: wyang@hkucc.hku.hk | en_HK |
dc.identifier.email | Lui, WY: wylui@hku.hk | - |
dc.identifier.authority | Lui, WY=rp00756 | en_HK |
dc.description.nature | link_to_subscribed_fulltext | - |
dc.identifier.doi | 10.1016/j.ejca.2012.04.016 | en_HK |
dc.identifier.pmid | 22647687 | - |
dc.identifier.scopus | eid_2-s2.0-84869502116 | en_HK |
dc.identifier.hkuros | 206216 | en_US |
dc.identifier.volume | 48 | - |
dc.identifier.issue | 18 | - |
dc.identifier.spage | 3475 | - |
dc.identifier.epage | 3487 | - |
dc.identifier.eissn | 1879-0852 | - |
dc.identifier.isi | WOS:000311218100017 | - |
dc.publisher.place | United Kingdom | en_HK |
dc.identifier.scopusauthorid | Lui, WY=35220192400 | en_HK |
dc.identifier.scopusauthorid | Wang, Y=7601513691 | en_HK |
dc.identifier.citeulike | 10726906 | - |
dc.identifier.issnl | 0959-8049 | - |