Cell-Cell Adhesion and Breast Cancer.
Annual rept. 15 Dec 97-14 Dec 98
GEORGETOWN UNIV WASHINGTON DC
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The objective of this proposal is to elucidate the role of cell-cell adhesion and calcium dependent cell adhesion molecules cadherins in breast tumor progression. We will test the hypothesis that in addition to the occasional loss of E-cadherin expression, breast tumor progression is more realistically modeled by a loss of strong cell-cell adhesion resulting from defects in any one or more of the steps molecules required for E-cadherin function. During the past year we have we published findings showing that invasive E-cadherin negative breast cancer cells express the mesenchymal cadherin, cadherin 11 which may well contribute to the invasive phenotype. Retinoid treatment was found to directly regulate Beta-cateninLEF signaling in a manner independent of cadherin function. We showed for the first time that Beta-catenin regulates contact inhibition, anchorage independent growth, anoikis and radiation-induced growth arrest. The tumor suppressor gene APC was shown to regulate Beta-catenin ubiquitination and degradation.
- Anatomy and Physiology
- Medicine and Medical Research