转移性激素敏感性前列腺癌转变为转移性去势抵抗性前列腺癌机制的研究进展  

Research progress on the transition metchansim of metastatic hormonesensitive prostate cancer to metastatic castration-resistant prostate cancer

作　　者：毛云 杨杰[1] 金坤 李晴 李树人[1] 李文泽[1] MAO Yun;YANG Jie;JIN Kun;LI Qing;LI Shuren;LI Wenze(Department of Urology,The First People’s Hospital of Xiangtan City,Xiangtan 411100,Hunan Province,China)

机构地区：[1]湘潭市第一人民医院泌尿外科,湖南湘潭411100

出　　处：《医学新知》2025年第2期222-231,共10页New Medicine

基　　金：湖南省湘潭市医学会科研项目(2024-xtyx-54)。

摘　　要：前列腺癌被诊断时大多已发生远处转移。雄激素剥夺疗法是治疗转移性激素敏感性前列腺癌(metastatic hormone-sensitive prostate cancer,mHSPC)的有效手段,但大多数患者最终发展为转移性去势抵抗性前列腺癌(metastatic castration-resistant prostate cancer,mCRPC)。调控mCRPC进展的机制尚不清楚,雄激素受体(androgen receptor,AR)信号传导已被证明在mCRPC中通过基因突变、过表达、共调节因子、AR剪切变异体和雄激素从头合成等发挥重要作用。越来越多的非AR通路也被证明影响mCRPC的进展,包括Wnt和Hedgehog通路。此外,非编码RNA、免疫相关机制和表观遗传修饰同样在mCRPC发病中扮演重要角色。据此,本文对mHSPC转变为mCRPC的相关机制作一综述,以期为相关研究提供参考。By the time prostate cancer is diagnosed,most cases have metastasized.Androgen-deprivation therapy is an effective means of treating metastatic hormone-sensitive prostate cancer(mHSPC),but most patients eventually develop to metastatic castrationresistant prostate cancer(mCRPC).The mechanisms regulating the progression of mCRPC are still unclear,and androgen receptor(AR)signaling has been shown to play an important role in mCRPC through AR gene mutations,overexpression,co-regulatory factors,AR splice variants,and androgen resynthesis.A growing number of non-AR pathways have also been shown to affect the progression of mCRPC,including the Wnt and Hedgehog pathways.In addition,non-coding RNAs,immune related mechanisms and epigenetic modifications also play important roles in the pathogenesis of mCRPC.This article reviewed the relevant transition mechanism of mHSCP to mCRPC,in order to provide reference for related research.

关 键 词：转移性前列腺癌 去势抵抗 雄激素受体 信号通路 非编码RNA 免疫调节 表观遗传修饰 

分 类 号：R737.25[医药卫生—肿瘤]