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Conference Paper: An angiogenic role of E-cadherin-positive exosomes in ovarian cancer

TitleAn angiogenic role of E-cadherin-positive exosomes in ovarian cancer
Authors
KeywordsMedical sciences
Oncology
Issue Date2015
PublisherAmerican Association for Cancer Research. The Journal's web site is located at http://cancerres.aacrjournals.org/
Citation
The 106th Annual Meeting of the American Association for Cancer research (AACR 2015), Philadelphia, PA., 18-22 April 2015. In Cancer Research, 2015, v. 75 n. 15 suppl., abstract no. 1035 How to Cite?
AbstractAngiogenesis, the induction of vasculature, is a vital step for metastasis. Loss of E-cadherin is a well-established marker for tumor metastasis. In ovarian cancer, a highly metastatic tumor that is rapidly lethal, we and others have previously shown the deregulated pattern of E-cadherin and its close association with tumor progression. Although E-cadherin is synthesized as a transmembrane molecule, it can be shed from the cell surface (sE-cad) which accounts for a rapid removal of functional E-cadherin. Here, in addition to ectodomain shedding, we show for the first time that sE-cad can be actively released from ovarian cancer cells in the form of exosomes. These sE-cad-positive exosomes play a critical role in angiogenesis which stimulated the migration, permeability, and tubulogenesis of human umbilical vein endothelial cells in vitro, and promoted functional neovascularization in vivo. In search of the underlying mechanisms by which sE-cad-positive exosomes might regulate angiogenic endothelial cells, which lack E-cadherin, we showed that a novel heterophilic crosstalk between sE-cad and VE-cadherin. Moreover, such angiogenic effect was mediated through activation of the phosphatidylinositol 3-kinase/Akt-beta-catenin signaling cascade. These results uncover a new angiogenic function for sE-cad and a novel paradigm for sE-cad production which may have potential clinical implications (This study was supported by RGC grant HKU781013). ©2015 American Association for Cancer Research.
DescriptionMeeting Theme: Bringing Cancer Discoveries to Patients
Session - Molecular and Cellular Biology: Poster session - Cell Signaling in Cancer 2: abstract no. 1035
This journal suppl. entitled: Proceedings: AACR 106th Annual Meeting 2015
Persistent Identifierhttp://hdl.handle.net/10722/213536
ISSN
2015 Impact Factor: 8.556
2015 SCImago Journal Rankings: 5.372

 

DC FieldValueLanguage
dc.contributor.authorTang, MKS-
dc.contributor.authorWong, AST-
dc.date.accessioned2015-08-05T02:57:07Z-
dc.date.available2015-08-05T02:57:07Z-
dc.date.issued2015-
dc.identifier.citationThe 106th Annual Meeting of the American Association for Cancer research (AACR 2015), Philadelphia, PA., 18-22 April 2015. In Cancer Research, 2015, v. 75 n. 15 suppl., abstract no. 1035-
dc.identifier.issn0008-5472-
dc.identifier.urihttp://hdl.handle.net/10722/213536-
dc.descriptionMeeting Theme: Bringing Cancer Discoveries to Patients-
dc.descriptionSession - Molecular and Cellular Biology: Poster session - Cell Signaling in Cancer 2: abstract no. 1035-
dc.descriptionThis journal suppl. entitled: Proceedings: AACR 106th Annual Meeting 2015-
dc.description.abstractAngiogenesis, the induction of vasculature, is a vital step for metastasis. Loss of E-cadherin is a well-established marker for tumor metastasis. In ovarian cancer, a highly metastatic tumor that is rapidly lethal, we and others have previously shown the deregulated pattern of E-cadherin and its close association with tumor progression. Although E-cadherin is synthesized as a transmembrane molecule, it can be shed from the cell surface (sE-cad) which accounts for a rapid removal of functional E-cadherin. Here, in addition to ectodomain shedding, we show for the first time that sE-cad can be actively released from ovarian cancer cells in the form of exosomes. These sE-cad-positive exosomes play a critical role in angiogenesis which stimulated the migration, permeability, and tubulogenesis of human umbilical vein endothelial cells in vitro, and promoted functional neovascularization in vivo. In search of the underlying mechanisms by which sE-cad-positive exosomes might regulate angiogenic endothelial cells, which lack E-cadherin, we showed that a novel heterophilic crosstalk between sE-cad and VE-cadherin. Moreover, such angiogenic effect was mediated through activation of the phosphatidylinositol 3-kinase/Akt-beta-catenin signaling cascade. These results uncover a new angiogenic function for sE-cad and a novel paradigm for sE-cad production which may have potential clinical implications (This study was supported by RGC grant HKU781013). ©2015 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 role of E-cadherin-positive exosomes 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.AM2015-1035-
dc.identifier.hkuros247720-
dc.identifier.volume75-
dc.identifier.issue15 suppl.-
dc.publisher.placeUnited States-

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