Since mutations in β-catenin, APC, and other components of the destruction complex appear very rarely in prostate cancer cells [17–19], our data from both in vitro and in vivo experimental approaches provide scientific evidence to elucidate a novel molecular mechanism underlying E-cadherin in regulating β-catenin cellular localization, and activity in promoting oncogenic transformation and cell growth in prostate cancer cells. This evidence concerns the gene APC and prostate cancer.