Control of Carcinoma Cell Motility by E-Cadherin
Abstract
Tumor invasion is a major obstacle to effective clinical management of breast cancer. To identify new targets for anti-invasive therapies, we have focused on the mechanisms by which the cell adhesion molecule E-cadherin suppresses tumor invasion. We previously found that E-cadherin does not suppress invasion via its adhesive activity. We hypothesized instead that E-cadherin-mediated contact generates intracellular signal(s) that regulate cell movement. In the present work, we have identified pathways by which E-cadherin affects cell behavior. In one pathway, cell-cell adhesion mediated by E- cadherin allows binding between the receptor tyrosine kinase EphA2 and its ligands. This interaction results in tyrosine phosphorylation of EphA2, which inhibits proliferation and decreases focal adhesions. The second pathway is defined by preliminary evidence suggesting that E-cadherin induces tyrosine phosphorylation of unidentified cell components by an EphA2-independent mechanism.
Document Details
- Document Type
- Technical Report
- Publication Date
- Aug 01, 1999
- Accession Number
- ADA385384
Entities
People
- Robert Brackenbury
Organizations
- University of Cincinnati