Prostate cancer (PC) is the second most common cause of cancer-related mortality in men in the western world after lung cancer. Many patients are not candidates for resection given the advanced stage of their cancer. The primary treatment for advanced PC is the castration therapy which supresses the production of androgens, hormone that promotes PC growth. Despite the efficiency of the castration therapy, most patients develop castration resistant disease which remains uncurable. Clearly, novel approaches are required to effectively treat castration resistant PC (CRPC). New strategies that identify the molecular mechanisms by which PC becomes resistant to conventional therapies may enable the identification of novel therapeutic targets that could improve clinical outcome. Recent studies have demonstrated the implication of TCTP's over-expression in PC and CRPC, and its role in resistance to treatment. TCTP's interaction with p53 and their negative feedback loop regulation have also been described to be causal for PC progression and invasion. A novel nanotherapy that inhibits TCTP has been developed as a new therapeutical strategy in CRPC. This chapter will highlight the role of TCTP as new therapeutic target in PC, in particular, therapy-resistant advanced PC and report the development of novel nanotherapy against TCTP that restore treatment-sensitivity in CRPC that deserve to be tested in clinical trial.
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