Protein modification with small ubiquitin-like modifiers (SUMOs) plays dual roles in prostate cancer (PCa) tumorigenesis and development. Any intermediary of the SUMO conjugation cycle going awry may forfeit the balance between tumorigenic potential and anticancer effects. Deregulated SUMOylation on the androgen receptor and oncoproteins also takes part in this pathological process, as exemplified by STAT3/NF-κB and tumor suppressors such as PTEN and p53. Here, we outline recent developments and discoveries of SUMOylation in PCa and present an overview of its multiple roles in PCa tumorigenesis/promotion and suppression, while elucidating its potential as a therapeutic target for PCa.

小泛素样修饰物 (SUMO) 的蛋白质修饰在前列腺癌 (PCa) 肿瘤发生和发展中发挥双重作用。 SUMO 结合周期的任何中间环节出错都可能会丧失致瘤潜力和抗癌作用之间的平衡。雄激素受体和癌蛋白上的 SUMO 化失调也参与了这一病理过程，例如 STAT3/NF-κB 和肿瘤抑制因子（例如 PTEN 和 p53）。在此，我们概述了 PCa 中 SUMO 化的最新进展和发现，并概述了其在 PCa 肿瘤发生/促进和抑制中的多重作用，同时阐明了其作为 PCa 治疗靶点的潜力。