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 found that a related cadherin, N-cadherin, does not suppress cell movement, even though it is as effective as E-cadherin at mediating adhesion. We have exploited this difference between E- and N-cadherin to define the region of E-cadherin required for suppression of movement. By constructing and analyzing a series of chimeric cadherins, consisting of parts of E- and N-cadherin, we localized the key region to a small portion of E-cadherin that includes the transmembrane segment. This unexpected result raises the possibility that clustering of E-cadherin may play a key role in triggering signals that affect cell movement and invasion.
Document Details
- Document Type
- Technical Report
- Publication Date
- Aug 01, 2000
- Accession Number
- ADA389845
Entities
People
- Robert Brackenbury
Organizations
- University of Cincinnati