Dissecting multiple roles of SUMOylation in prostate cancer

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-kappa B 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.

Automated summary

Protein modification with SUMOs has dual roles in prostate cancer tumorigenesis and development, with deregulated SUMOylation affecting the balance between tumorigenic potential and anticancer effects. SUMOylation on the androgen receptor and oncoproteins plays a role in this pathological process in PCa.