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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
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- Reddy, Pradeep (author)
- Umeå universitet,Institutionen för medicinsk kemi och biofysik
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- Liu, Lian (author)
- Umeå universitet,Institutionen för medicinsk kemi och biofysik
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- Ren, Chong (author)
- Umeå universitet,Institutionen för medicinsk kemi och biofysik
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- The Endocrine Society, 2005
- 2005
- English.
- In: Mol Endocrinol. - : The Endocrine Society. - 0888-8809. ; 19:10, s. 2564-2578
- Journal article (peer-reviewed)
Abstract
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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.
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- Reddy, Pradeep
- Liu, Lian
- Ren, Chong
- Lindgren, Peter
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- Lundin, Eva
- Ottander, Ulrika
- Rytinki, Miia
- Liu, Kui
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