Cadherins participate in calcium-dependent cell-cell adhesion. Although numerous models have been proposed for cadherin-cadherin interactions, the exact mechanism remains elusive. Structural and mutational analyses have emphasized the importance of the N-terminus and the HAV domain, and have determined that specificity of cadherin interaction is determined by amino acids in the 1st cadherin repeat. E-cadherin expression is irreversibly lost in invasive lobular cancer (ILC) and epigenetic alterations in cadherins frequently accompany ductal breast carcinomas. Animal models of lobular cancer provide mechanistic insight into the role of E-cadherin as a tumor and invasion suppressor in ILC. Transcriptional regulators of E-cadherin that act as master regulators of epithelial-mesenchymal transition in development have been identified. Mis-expression of cadherins promotes a migratory phenotype in breast cancer. E-cadherin binding partners, such as β-catenin and p120ctn, that participate in cell signaling, are lost or mislocalized in tumors lacking cadherins. In conclusion, cadherins act as suppressors of invasion and metastasis through multiple routes.
- Epithelial-mesenchymal transition.
Available at: http://works.bepress.com/minoti_hiremath/2/