Nat. Rev. Urol. doi: /nrurol

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Nat. Rev. Urol. doi:10.1038/nrurol.2015.254 Figure 3 Androgen action in a castration resistant prostate cancer cell via AR– ARE binding and potential consequences of enzalutamide blockade Figure 3 | Androgen action in a castration resistant prostate cancer cell via AR– ARE binding and potential consequences of enzalutamide blockade. In castration-resistant prostate cancer (CRPC), androgens bind the androgen receptor (AR), leading to dimerization and nuclear translocation followed by binding of the AR dimer to androgen response elements (AREs) in the promoter or distal sites of androgen target genes to activate AR pathways. In patients with enzalutamide-sensitive CRPC, enzalutamide binding to the AR prevents active androgen binding, thereby inhibiting AR action. The enzalutamide–AR complex is less able to translocate from cytoplasm to nucleus and, therefore, fails to activate target genes, leading to androgen deprivation and inhibition of prostate cancer growth. In one potential pathway leading to enzalutamide resistance, enzalutamide blockade of androgen action removes the normal androgen inhibition of GRs leading to elevated glucocorticoid receptor (GR) expression. These GRs, in complexes with cortisol or administered glucocorticoids, can then bind to AREs and co-opt regulation of some of the classical AR target genes, causing prostate cancer growth and enzalutamide resistance. Narayanan, S. et al. (2015) Androgen–glucocorticoid interactions in the era of novel prostate cancer therapy Nat. Rev. Urol. doi:10.1038/nrurol.2015.254