相扑蛋白
前列腺癌
癌变
癌症研究
PTEN公司
雄激素受体
肿瘤促进
泛素
生物
癌症
细胞生物学
信号转导
PI3K/AKT/mTOR通路
生物化学
遗传学
基因
标识
DOI:10.1016/j.canlet.2021.08.034
摘要
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.
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