Abstract

Prostate cancer is the most frequently diagnosed non-cutaneous cancer and the second leading cause of cancer death in the male population in the USA and other developed nations. Initially, prostate cancer is dependent on androgens for growth, which provides a basis for using androgen deprivation therapy to treat locally advanced or metastatic disease. However, prostate cancer almost always progresses to a castration-resistant phenotype for which few treatment options with improved overall survival are available at present. Multiple studies have shown that active androgen receptor (AR) signaling is still required for development, growth, and progression of castration-resistant prostate cancer (CRPC). Thus, targeting AR signaling, particularly androgen-independent activation of AR signaling, in CRPC may result in novel therapeutic strategies. In this chapter, we summarize recent findings on the regulation of AR signaling by histone deacetylase 6 (HDAC6) and discuss the potential mechanisms by which HDAC6 influences androgen signaling in prostate cancer. We also discuss the potential of targeting HDAC6 in prostate cancer treatment.KeywordsProstate CancerAndrogen ReceptorProstate Cancer CellHDAC InhibitorAndrogen Receptor SignalingThese keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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