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Conference Paper: A correlation between TGF-β1-mediated JAM-A downregulation and cell invasiveness

TitleA correlation between TGF-β1-mediated JAM-A downregulation and cell invasiveness
Authors
KeywordsBiology
Biochemistry
Issue Date2010
PublisherWiley-Blackwell Publishing Ltd.. The Journal's web site is located at http://www.febsjournal.org/
Citation
The 35th FEBS Congress, Gothenburg, Sweden, 26 June-1 July 2010. In The FEBS Journal, 2010, v. 277 suppl. 1, p. 144 How to Cite?
AbstractTransforming growth factor-beta (TGF-β) and junctional adhesion molecule-A (JAM-A) have been indicated as key regulators of cell migration, and an inverse relationship of JAM-A expression and the invasiveness has been reported in breast cancer cells. Whether TGF- β1 signaling induces JAM-A downregulation leading to cancer cell invasion has not been investigated. In this study, we report that TGF- β1 significantly downregulates JAMA expression at both mRNA and protein levels in MCF-7 cells that is slightly migratory and normally expresses high level of JAM-A. We showed that TGF-β1 downregulates JAM-A mRNA level via transcriptional regulation and the promoter region responsible to TGF-β1 stimulation is located between nt -367 and -1. In addition, TGF-β1 exerted its negative effect on JAMA expression via post-translational control. There was a significant reduction (60% reduction) in JAM-A protein levels in cyclohexamide-pretreated TGF-β1-treated cells, indicating that TGF-β1 promotes JAM-A protein turnover. We showed that JNK inhibitor, but not Smad3 and Smad4 siRNA, could effectively abolish TGF-β1-mediated JAM-A protein degradation, although Smad activation alone could abolish JAM-A degradation in the absence of TGF-β1 stimulation. Furthermore, clathrin siRNA abolished TGF-β1-mediated JAM-A degradation, indicating that the degradation is mediated via clathrin-dependent endocytosis. Reduction of JAM-A in MCF-7 cells upon TGF-β1 treatment led to enhanced invasion in the invasion assays. Taken together, these results indicate a strong correlation between TGF-β1-mediated JAM-A downregulation and cell invasiveness.
DescriptionThis is the Special issue: Abstracts of the 35th FEBS Congress
Poster Presentation: B2 - Signal Transduction: abstract no. B2.92
Persistent Identifierhttp://hdl.handle.net/10722/130261
ISSN
2015 Impact Factor: 4.237
2015 SCImago Journal Rankings: 2.141

 

DC FieldValueLanguage
dc.contributor.authorWang, Yen_US
dc.contributor.authorLui, WYen_US
dc.date.accessioned2010-12-23T08:48:32Z-
dc.date.available2010-12-23T08:48:32Z-
dc.date.issued2010en_US
dc.identifier.citationThe 35th FEBS Congress, Gothenburg, Sweden, 26 June-1 July 2010. In The FEBS Journal, 2010, v. 277 suppl. 1, p. 144en_US
dc.identifier.issn1742-464X-
dc.identifier.urihttp://hdl.handle.net/10722/130261-
dc.descriptionThis is the Special issue: Abstracts of the 35th FEBS Congress-
dc.descriptionPoster Presentation: B2 - Signal Transduction: abstract no. B2.92-
dc.description.abstractTransforming growth factor-beta (TGF-β) and junctional adhesion molecule-A (JAM-A) have been indicated as key regulators of cell migration, and an inverse relationship of JAM-A expression and the invasiveness has been reported in breast cancer cells. Whether TGF- β1 signaling induces JAM-A downregulation leading to cancer cell invasion has not been investigated. In this study, we report that TGF- β1 significantly downregulates JAMA expression at both mRNA and protein levels in MCF-7 cells that is slightly migratory and normally expresses high level of JAM-A. We showed that TGF-β1 downregulates JAM-A mRNA level via transcriptional regulation and the promoter region responsible to TGF-β1 stimulation is located between nt -367 and -1. In addition, TGF-β1 exerted its negative effect on JAMA expression via post-translational control. There was a significant reduction (60% reduction) in JAM-A protein levels in cyclohexamide-pretreated TGF-β1-treated cells, indicating that TGF-β1 promotes JAM-A protein turnover. We showed that JNK inhibitor, but not Smad3 and Smad4 siRNA, could effectively abolish TGF-β1-mediated JAM-A protein degradation, although Smad activation alone could abolish JAM-A degradation in the absence of TGF-β1 stimulation. Furthermore, clathrin siRNA abolished TGF-β1-mediated JAM-A degradation, indicating that the degradation is mediated via clathrin-dependent endocytosis. Reduction of JAM-A in MCF-7 cells upon TGF-β1 treatment led to enhanced invasion in the invasion assays. Taken together, these results indicate a strong correlation between TGF-β1-mediated JAM-A downregulation and cell invasiveness.-
dc.languageengen_US
dc.publisherWiley-Blackwell Publishing Ltd.. The Journal's web site is located at http://www.febsjournal.org/-
dc.relation.ispartofThe FEBS Journal-
dc.rightsThe definitive version is available at www3.interscience.wiley.com-
dc.subjectBiology-
dc.subjectBiochemistry-
dc.titleA correlation between TGF-β1-mediated JAM-A downregulation and cell invasivenessen_US
dc.typeConference_Paperen_US
dc.identifier.emailWang, Y: wyang@hkucc.hku.hken_US
dc.identifier.emailLui, WY: wylui@hku.hken_US
dc.identifier.authorityLui, WY=rp00756en_US
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1111/j.1742-4658.2010.07680.x-
dc.identifier.hkuros176570en_US
dc.identifier.volume277-
dc.identifier.issuesuppl. 1-
dc.identifier.spage144-
dc.identifier.epage144-
dc.publisher.placeUnited Kingdom-
dc.description.otherThe 35th FEBS Congress, Gothenburg, Sweden, 26 June-1 July 2010. In The FEBS Journal, 2010, v. 277 suppl. 1, p. 144-

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