醛酮还原酶AKR1C3促进前列腺癌进展、转移和耐药的研究进展  

Current Study on the Mechanism in AKR1C3 Promoting Prostate Cancer Progress,Metastasis and Drug Resistance

作　　者：严婧 姚洲 李方琪 张琦[1] 钟文韬[1] 李晶[2] Yan Jing;Yao Zhou;Li Fangqi;Zhang Qi;Zhong Wentao;Li Jing(The Second Bethune Clinical Medicine College of Jilin University,Changchun 130021;Department of Pharmacology,College of Basic Medical Sciences,Jilin University,Changchun 130021)

机构地区：[1]吉林大学白求恩第二临床医学院,长春130021 [2]吉林大学基础医学院药理学系,长春130021

出　　处：《国际老年医学杂志》2022年第4期476-479,共4页International Journal of Geriatrics

基　　金：吉林省发展改革委员会产业技术研究与开发专项(2020C034-2);吉林大学大学生创新训练计划省级项目(201910183809)。

摘　　要：前列腺癌是男性高发癌症,雄激素剥夺治疗(ADT)后易发展为去势抵抗性前列腺癌(CRPC),经免疫组化和标本活检发现癌细胞内雄激素的再次增多是导致CRPC的主要原因之一。2型3α-羟基类固醇脱氢酶醛酮还原酶(AKR1C3)与CRPC细胞中雄激素自身合成途径密切相关,并促进CRPC进展为耐药或转移侵袭,因此靶向抑制AKR1C3可治疗CRPC。本文对AKR1C3在前列腺癌进展、转移和耐药中的作用机制及新型AKR1C3抑制剂对CRPC的治疗作一综述。Prostate cancer is a high incidence of cancer in the males.It is easy to develop into castrated resistant prostate cancer(CRPC)after androgen deprivation therapy(ADT).The increase of androgen in prostate cancer is one of the main mechanisms leading to CRPC detected by immunohistochemistry and biopsy.Type 23α-hydroxyl steroid dehydrogenase aldosterone reductase(AKR1 C3)is closely related to androgen self-synthesis pathway in CRPC cells and promotes the development of drug resistance and metastasis.AKR1 C3 has been proved a target in the treatment of CRPC.The role of AKR1 C3 in the progress,metastasis and drug resistance of prostate cancer and the mechanism of new AKR1 C3 inhibitors is being reviewed.

关 键 词：2型3α-羟基类固醇脱氢酶醛酮还原酶 去势抵抗性前列腺癌 雄激素 抑制剂 

分 类 号：R737.25[医药卫生—肿瘤]