Figure 1

Contribution of EMT, CSC and related signaling to CRPC. Castration induces EMT and enhances the stemness of CSCs, which are the two key contributors for the development of castration resistance. Following castration, epithelial cells lose their epithelial phenotypes, i.e., biomarkers such as E-cadherin, but gain mesenchymal characteristics or biomarkers such as N-cadherin and Zeb-1. Cancer stem cells are stem cell-like tumor cells, which have the capability of self-renewal and differentiation. Castration can enrich this population. Certain molecules might be regarded as prostate cancer stem cell markers, such as CD133, CD166, and etc. Specific signaling including Wnt, Notch, SHH, and others might be the underlying molecular basis of the functions of EMT and CSCs. The EMT appears to be a dynamic process. Development of drugs either inhibiting EMT, CSCs and specific signaling pathways or enhancing expression of epithelial cell markers might be a novel, additional strategy to treat CRPC in the future. (→, Promote; ⊥, Inhibit.)