The Role of E-Cadherin-Catenin Complex in Prostate Cancer Progression

The genetic changes that promote progression of prostate adenocarcinomas are multifactori‐ al and include alterations in several genes. The aberrations include those in genes that affect normal cell adhesion. The long arm of chromosome 16 (16q22.1) is deleted in 30% of primary prostatic tumors and more than 70% of metastatic prostate cancers. The E-cadherin gene is located in this region. E-cadherin is involved in maintaining homotypic cell-cell adhesion between normal prostatic glandular cells. The loss of E-cadherin expression is associated with metastatic progression of prostate cancer (Mason, 2002). Recent data suggests that ab‐ normal expression of E-cadherin, leading to impaired adhesion, correlates with hematoge‐ nous spread of primary tumor cells in prostate cancer patients (Loric, 2001). The study further suggests that abnormal E-cadherin expression is a significant independent indicator of prostate cancer recurrence in patients.