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Article: Formation of E-cadherin-mediated cell-cell adhesion activates akt and mitogen activated protein kinase via phosphatidylinositol 3 kinase and ligand-independent activation of epidermal growth factor receptor in ovarian cancer cells

TitleFormation of E-cadherin-mediated cell-cell adhesion activates akt and mitogen activated protein kinase via phosphatidylinositol 3 kinase and ligand-independent activation of epidermal growth factor receptor in ovarian cancer cells
Authors
Issue Date2005
Citation
Molecular Endocrinology, 2005, v. 19, n. 10, p. 2564-2578 How to Cite?
AbstractE-cadherin is a well characterized adhesion molecule that plays a major role in epithelial cell adhesion. Based on findings that expression of E-cadherin is frequently lost in human epithelial cancers, it has been implicated as a tumor suppressor in carcinogenesis of most human epithelial cancers. However, in ovarian cancer development, our data from the current study showed that E-cadherin expression is uniquely elevated in 86.5% of benign, borderline, and malignant ovarian carcinomas irrespective of the degree of differentiation, whereas normal ovarian samples do not express E-cadherin. Thus, we hypothesize that E-cadherin may play a distinct role in the development of ovarian epithelial cancers. Using an E-cadherin-expressing ovarian cancer cell line OVCAR-3, we have demonstrated for the first time that the establishment of E-cadherin mediated cell-cell adhesions leads to the activation of Akt and MAPK. Akt activation is mediated through the activation of phosphatidylinositol 3 kinase, and both Akt and MAPK activation are mediated by an E-cadherin adhesion-induced ligand-independent activation of epidermal growth factor receptor. We have also demonstrated that suppression of E-cadherin function leads to retarded cell proliferation and reduced viability. We therefore suggest that the concurrent formation of E-cadherin adhesion and activation of downstream proliferation signals may enhance the proliferation and survival of ovarian cancer cells. Our data partly explain why E-cadherin is always expressed during ovarian tumor development and progression. Copyright © 2005 by The Endocrine Society.
Persistent Identifierhttp://hdl.handle.net/10722/265764
ISSN
2017 Impact Factor: 3.678
2015 SCImago Journal Rankings: 2.195
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorReddy, Pradeep-
dc.contributor.authorLiu, Lian-
dc.contributor.authorRen, Chong-
dc.contributor.authorLindgren, Peter-
dc.contributor.authorBoman, Karin-
dc.contributor.authorShen, Yan-
dc.contributor.authorLundin, Eva-
dc.contributor.authorOttander, Ulrika-
dc.contributor.authorRytinki, Miia-
dc.contributor.authorLiu, Kui-
dc.date.accessioned2018-12-03T01:21:37Z-
dc.date.available2018-12-03T01:21:37Z-
dc.date.issued2005-
dc.identifier.citationMolecular Endocrinology, 2005, v. 19, n. 10, p. 2564-2578-
dc.identifier.issn0888-8809-
dc.identifier.urihttp://hdl.handle.net/10722/265764-
dc.description.abstractE-cadherin is a well characterized adhesion molecule that plays a major role in epithelial cell adhesion. Based on findings that expression of E-cadherin is frequently lost in human epithelial cancers, it has been implicated as a tumor suppressor in carcinogenesis of most human epithelial cancers. However, in ovarian cancer development, our data from the current study showed that E-cadherin expression is uniquely elevated in 86.5% of benign, borderline, and malignant ovarian carcinomas irrespective of the degree of differentiation, whereas normal ovarian samples do not express E-cadherin. Thus, we hypothesize that E-cadherin may play a distinct role in the development of ovarian epithelial cancers. Using an E-cadherin-expressing ovarian cancer cell line OVCAR-3, we have demonstrated for the first time that the establishment of E-cadherin mediated cell-cell adhesions leads to the activation of Akt and MAPK. Akt activation is mediated through the activation of phosphatidylinositol 3 kinase, and both Akt and MAPK activation are mediated by an E-cadherin adhesion-induced ligand-independent activation of epidermal growth factor receptor. We have also demonstrated that suppression of E-cadherin function leads to retarded cell proliferation and reduced viability. We therefore suggest that the concurrent formation of E-cadherin adhesion and activation of downstream proliferation signals may enhance the proliferation and survival of ovarian cancer cells. Our data partly explain why E-cadherin is always expressed during ovarian tumor development and progression. Copyright © 2005 by The Endocrine Society.-
dc.languageeng-
dc.relation.ispartofMolecular Endocrinology-
dc.titleFormation of E-cadherin-mediated cell-cell adhesion activates akt and mitogen activated protein kinase via phosphatidylinositol 3 kinase and ligand-independent activation of epidermal growth factor receptor in ovarian cancer cells-
dc.typeArticle-
dc.description.natureLink_to_OA_fulltext-
dc.identifier.doi10.1210/me.2004-0342-
dc.identifier.pmid15928314-
dc.identifier.scopuseid_2-s2.0-25444448222-
dc.identifier.volume19-
dc.identifier.issue10-
dc.identifier.spage2564-
dc.identifier.epage2578-
dc.identifier.isiWOS:000232116900012-

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