Role of E-Cadherin Homophilic Contacts in the Inhibition of Cell Growth of Primary Breast Cells
Abstract
At present, it remains obscure whether E-cadherin directly transfers growth inhibitory signals to the cells, or if other types of molecular cell interactions indirectly influenced by the establishment of cadherin mediated cell contacts, are responsible for contact inhibition of growth. In this study I selectively activate the formation of E-cadherin homophilic adhesive bonds, using a specific recombinant protein to engage E-cadherin molecules at the cell surface of primary epithelial cells. My previous data demonstrated that E-cadherin is capable of transducing a growth inhibitory signal independent of other cell-cell interactions. Moreover, my previous data also shows that this event is not mediated through a Wnt/beta-catenin signaling antagonism. This has directed me to analyze the relationship between the association of p120(exp ctn) with E cadherin and the inhibition of cell growth. We have successfully generated E-cadherin Deltal2O transgenic mice, and pl2O conditional KO mice in skin and mammary epithelia to study the consequences of the loss of the interaction of p120 with E-cadherin in vivo. In addition using a yeast-two hybrid screen I have identified novel interacting partners of pl20(exp ctn) that can be potentially involved in transducing growth inhibitory signals to the cells.
Document Details
- Document Type
- Technical Report
- Publication Date
- Aug 01, 2004
- Accession Number
- ADA430025
Entities
People
- Elaine Fuchs
- Mirna Perez-moreno
Organizations
- The Rockefeller University