Fig. 5: Inhibition of UHRF1 demonstrates potential therapeutic value in the treatment of advanced prostate cancer.

A Representative images of tumors derived from NC- and UHRF-knockdown cells. B Growth curves of cell-derived xenografts (CDX) in tumors derived from NC and UHRF1 knockdown cells. C Immunohistochemical staining of UHRF1, and Ki67 in tumor tissues derived from NC and UHRF1 knockdown cells. D Proposed model: UHRF1 promotes the ubiquitination of AR, thereby facilitating its degradation and promoting cancer cell proliferation through AR-independent compensatory mechanisms, thus contributing to tumor treatment resistance.