In support of these observations, reducing either β-catenin or AR expression using specific shRNA lentiviruses significantly attenuated androgen-induced AR-mediated transcriptional activity onset by E-cadherin knockdown in cells, providing evidence of a direct role of β-catenin in enhancing AR transcriptional activity in E-cadherin null prostate cancer cells (Fig 3I). The gene discussed is CDH1; the disease is prostate carcinoma.