Cadherins are a class of cell surface proteins that function in maintaining tissue organization, intercellular communication, and cytoskeletal integrity. The loss of cadherin in prostate cancer predicts for a poor prognosis and malignancy. A goal of our laboratory is to investigate the molecular role of cadherin in tumor progression and regulating cellular function. The expression of the cadherin gene in a prostate cancer line facilitated intercellular contact, redistribution of the actin cytoskeleton, and growth suppression. Alteration of the extracellular portion of the molecule eliminates cell contact but retains growth suppression. In contrast the truncation of the cytoplasmic portion cell contact is unaffected but the growth suppressive activity is lost. In addition, the reorganization of the actin cytoskeleton and the redistribution of beta-catenin mediated by cadherin are closely associated with the growth suppressive activity. These findings suggest that the growth suppressive property of cadherin involves the alteration of the cytoskeleton and perhaps intracellular signaling. To address these possibilities, the laboratory focus is on the alteration of catenin proteins, which link the cadherin to the actin cytoskeleton. The disassociation of cadherin with the actin cytoskeleton should result in the loss of cadherin mediated growth suppression. Furthermore, it is predicted that the regulation of genes involved in growth suppression will be affected with cadherin expression and analysis of differential gene expression will be investigated
