Together, these results indicate that NURR1 could function to enhance the castration-resistant growth of prostate cancer cells in vivo, mediated through its activation of β-catenin activity accompanied with enhanced EMT and cancer stemness; and also targeting Wnt signaling could suppress the NURR1-induced castration-relapse tumor growth of prostate cancer. The gene discussed is NR4A2; the disease is prostate carcinoma.