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作 者:孙国良 王之泽 叶章群[1] 李恒[1] Sun Guoliang;Wang Zhize;Ye Zhangqun;Li Heng(Departments of Urology,Tongji Hospital,Tongji Medical College,Huazhong University of Science and Technology,Wuhan 430030,China;Department of Urology,the First Affiliated Hospital,School of Medicine,Zhejiang University,Hangzhou 310000,China)
机构地区:[1]华中科技大学同济医学院附属同济医院泌尿外科,武汉430030 [2]浙江大学医学院附属第一医院泌尿外科,杭州310000
出 处:《中华实验外科杂志》2019年第6期1161-1166,共6页Chinese Journal of Experimental Surgery
摘 要:到去势抵抗,并对二代内分泌药物治疗具有耐药性的机制之一。因此,AR-V7作为前列腺癌潜在的治疗靶标,其上游调控方式已经成为了一个新的研究热点。目前的研究表明,AR-V7的表达水平和转录活性受到转录因子、共激活因子、剪接因子、RNA结合蛋白、酶类、热休克蛋白、溴结构域蛋白4、长链非编码RNA和聚腺苷酸化信号等因素的调控。本文综述了AR-V7与前列腺癌的关系及AR-V7上游调控方式的相关研究进展。Androgen receptor splice variant 7 (AR-V7) is one of the androgen receptor splice variants, which is highly expressed in castration-resistant prostate cancer tissues. Recent studies have showed that AR-V7 is one of the mechanisms of the progression of castration-resistant prostate cancer with the resistance of second generation hormonal therapy. Consequently, as a potential therapeutic target for prostate cancer, the upstream regulation of AR-V7 has become a new research hotspot. Current researches show that the expression level and transcriptional activity of AR-V7 are regulated by transcription factors, coactivators, splicing factors, RNA binding proteins, enzymes, heat shock proteins, bromodoma in-containing protein 4, long non-coding RNAs, polyadenylation signal, etc. This article reviews the relationship between AR-V7 and prostate cancer and the upstream regulation of AR-V7.
关 键 词:前列腺癌 雄激素受体剪接变异体7 上游调控方式
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