The conversion of the sessile epithelial cells to the motile mesenchymal phenotype (EMT transition) involves the characteristic switching of E-cadherin to N-cadherin and is a "signature-like event", involving the TGFβ1-mediated pathway, in the process of invasion and metastasis of prostate cancer cells -a process commonly observed in other cancer cells. The transcriptional epigenetic repression of E-cadherin is associated with and regulated by the expression of ZEB1 - zinc finger homeo-domain transcription repressor, which in turn, is regulated by specific microRNAs. The role of IGF-1, correlatable with ZEB1, through equivocal, may have an important staging-dependent differential role in prostate cancer. Other transcription factors (Snail, Slug & E-47), when expressed, induce, among other signaling molecules, the expression of IGF-1 and Wnt-5. This, in turn, causes E-cadherin repression. One of the major, common downstream pro-survival effector protein is PI3K/Akt and is regulated both by the Ras as well as the TGF-β pathways. This pivotal protein is known to protect the cells against TGFβ-mediated apoptosis and plays an important role in EMT and metastasis. Repression of E-cadherin, is accompanied by the Twist1-dependent expression of N-cadherin. Corroborative evidence supports the abnormal activation of the Wnt/β catenin pathway and this pathway has been strongly implicated in prostate cancer invasion and metastasis pathways while catenin-independent pathways have also been reported apart from important epigenetic mechanisms regulating the inhibitors of the pathway like (Wnt inhibitory factor-1 -WIF-1). This review provides the reader with an update on the role of important signaling molecules and a better molecular understanding of cadherin switching - lessons that can be applied in cancer biology and chemoprevention by ethno-pharmacological and bio-pharmaceutical approaches.