Search: onr:"swepub:oai:DiVA.org:umu-14563" >
Formation of E-cadh...
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Reddy, PradeepUmeå universitet,Institutionen för medicinsk kemi och biofysik
(author)
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
- Article/chapterEnglish2005
Publisher, publication year, extent ...
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The Endocrine Society,2005
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printrdacarrier
Numbers
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LIBRIS-ID:oai:DiVA.org:umu-14563
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https://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-14563URI
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https://doi.org/10.1210/me.2004-0342DOI
Supplementary language notes
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Language:English
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Summary in:English
Part of subdatabase
Classification
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Subject category:ref swepub-contenttype
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Subject category:art swepub-publicationtype
Notes
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E-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.
Added entries (persons, corporate bodies, meetings, titles ...)
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Liu, LianUmeå universitet,Institutionen för medicinsk kemi och biofysik
(author)
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Ren, ChongUmeå universitet,Institutionen för medicinsk kemi och biofysik
(author)
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Lindgren, PeterUmeå universitet,Obstetrik och gynekologi
(author)
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Boman, KarinUmeå universitet,Onkologi(Swepub:umu)kabo0010
(author)
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Shen, YanUmeå universitet,Institutionen för medicinsk kemi och biofysik
(author)
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Lundin, EvaUmeå universitet,Institutionen för medicinsk biovetenskap(Swepub:umu)evlu0001
(author)
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Ottander, UlrikaUmeå universitet,Obstetrik och gynekologi(Swepub:umu)ulaotr95
(author)
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Rytinki, MiiaUmeå universitet,Institutionen för medicinsk kemi och biofysik
(author)
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Liu, KuiUmeå universitet,Institutionen för medicinsk kemi och biofysik(Swepub:umu)kuli0001
(author)
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Umeå universitetInstitutionen för medicinsk kemi och biofysik
(creator_code:org_t)
Related titles
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In:Mol Endocrinol: The Endocrine Society19:10, s. 2564-25780888-8809
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In:Molecular Endocrinology: The Endocrine Society19:10, s. 2564-25781944-9917
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To the university's database
- By the author/editor
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Reddy, Pradeep
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Liu, Lian
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Ren, Chong
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Lindgren, Peter
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Boman, Karin
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Shen, Yan
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show more...
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Lundin, Eva
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Ottander, Ulrika
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Rytinki, Miia
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Liu, Kui
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- Articles in the publication
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Mol Endocrinol
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Molecular Endocr ...
- By the university
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Umeå University