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Conference Paper: An angiogenic function for E-cadherin in ovarian cancer

TitleAn angiogenic function for E-cadherin in ovarian cancer
Authors
KeywordsMedical sciences
Oncology
Issue Date2014
PublisherAmerican Association for Cancer Research. The Journal's web site is located at http://cancerres.aacrjournals.org/
Citation
The 2014 Annual Meeting of the American Association for Cancer research (AACR 2014), San Diego, CA., 5-9 April 2014. In Cancer Research, 2014, v. 74 n. 19 suppl., abstract no. 9 How to Cite?
AbstractThe loss of E-cadherin, a cell-cell adhesion molecule, is a well-established marker for metastasis of cancer. Although E-cadherin is synthesized as a transmembrane molecule, it can be cleaved of the ectodomain and released in a soluble form (sE-cad), and this accounts a key mechanism for a rapid reduction of functional E-cadherin at the cell surface. Yet, very little is known about how this important protein dictates the metastasis of these tumors. In ovarian cancer, a highly metastatic tumor that is rapidly lethal, sE-cad is highly expressed in the serum and metastatic ascites of ovarian carcinoma patients. Despite many studies focused on the role of E-cadherin loss in weakening cell-cell adhesion, whether sE-cad has biological activity in itself remain virtually unknown. Here we show for the first time that sE-cad can transduce angiogenic signals. sE-cad was also present in the culture supernatant of ovarian cancer lines. sE-cad of supernatant and a recombinant sE-cad-Fc chimera potently stimulated the migration of, permeability, and tubulogenesis by human umbilical vein endothelial cells in vitro. sE-cad also promoted functional neovascularization in a Matrigel implant model in vivo. These effects could be reversed by neutralizing anti-sE-cad, confirming that the effects were sE-cad specific. In addition, we found that sE-cad bound to VE-cadherin, an effect mediated through the phosphatidylinositol 3-kinase/Akt-β-catenin pathway. These results unravel a new and important piece to the complex biology of tumor angiogenesis and metastasis, and provide insights of novel mechanisms regulating angiogenesis. (This study was supported by RGC grant HKU781013). ©2014 American Association for Cancer Research.
DescriptionMeeting Theme: Harnessing Breakthroughs - Targeting Cures
Session - Tumor Biology: Poster Presentations - Angiogenesis 1: Molecular and Cellular Mechanisms: abstract no. 9
This journal suppl. entitled: Proceedings: AACR Annual Meeting 2014
Persistent Identifierhttp://hdl.handle.net/10722/213533
ISSN
2015 Impact Factor: 8.556
2015 SCImago Journal Rankings: 5.372

 

DC FieldValueLanguage
dc.contributor.authorTang, MKS-
dc.contributor.authorWong, AST-
dc.date.accessioned2015-08-05T02:24:51Z-
dc.date.available2015-08-05T02:24:51Z-
dc.date.issued2014-
dc.identifier.citationThe 2014 Annual Meeting of the American Association for Cancer research (AACR 2014), San Diego, CA., 5-9 April 2014. In Cancer Research, 2014, v. 74 n. 19 suppl., abstract no. 9-
dc.identifier.issn0008-5472-
dc.identifier.urihttp://hdl.handle.net/10722/213533-
dc.descriptionMeeting Theme: Harnessing Breakthroughs - Targeting Cures-
dc.descriptionSession - Tumor Biology: Poster Presentations - Angiogenesis 1: Molecular and Cellular Mechanisms: abstract no. 9-
dc.descriptionThis journal suppl. entitled: Proceedings: AACR Annual Meeting 2014-
dc.description.abstractThe loss of E-cadherin, a cell-cell adhesion molecule, is a well-established marker for metastasis of cancer. Although E-cadherin is synthesized as a transmembrane molecule, it can be cleaved of the ectodomain and released in a soluble form (sE-cad), and this accounts a key mechanism for a rapid reduction of functional E-cadherin at the cell surface. Yet, very little is known about how this important protein dictates the metastasis of these tumors. In ovarian cancer, a highly metastatic tumor that is rapidly lethal, sE-cad is highly expressed in the serum and metastatic ascites of ovarian carcinoma patients. Despite many studies focused on the role of E-cadherin loss in weakening cell-cell adhesion, whether sE-cad has biological activity in itself remain virtually unknown. Here we show for the first time that sE-cad can transduce angiogenic signals. sE-cad was also present in the culture supernatant of ovarian cancer lines. sE-cad of supernatant and a recombinant sE-cad-Fc chimera potently stimulated the migration of, permeability, and tubulogenesis by human umbilical vein endothelial cells in vitro. sE-cad also promoted functional neovascularization in a Matrigel implant model in vivo. These effects could be reversed by neutralizing anti-sE-cad, confirming that the effects were sE-cad specific. In addition, we found that sE-cad bound to VE-cadherin, an effect mediated through the phosphatidylinositol 3-kinase/Akt-β-catenin pathway. These results unravel a new and important piece to the complex biology of tumor angiogenesis and metastasis, and provide insights of novel mechanisms regulating angiogenesis. (This study was supported by RGC grant HKU781013). ©2014 American Association for Cancer Research.-
dc.languageeng-
dc.publisherAmerican Association for Cancer Research. The Journal's web site is located at http://cancerres.aacrjournals.org/-
dc.relation.ispartofCancer Research-
dc.subjectMedical sciences-
dc.subjectOncology-
dc.titleAn angiogenic function for E-cadherin in ovarian cancer-
dc.typeConference_Paper-
dc.identifier.emailTang, MKS: mkstang@hku.hk-
dc.identifier.emailWong, AST: awong1@hku.hk-
dc.identifier.authorityWong, AST=rp00805-
dc.identifier.doi10.1158/1538-7445.AM2014-9-
dc.identifier.hkuros247715-
dc.identifier.volume74-
dc.identifier.issue19 suppl.-
dc.publisher.placeUnited States-

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