Fancher Ashley T, Hua Yun, Strock Christopher J, Johnston Paul A
Department of Pharmaceutical Sciences, School of Pharmacy, University of Pittsburgh, Pittsburgh, Pennsylvania.
Cyprotex US, Watertown, Massachusetts.
Assay Drug Dev Technol. 2019 Nov/Dec;17(8):364-386. doi: 10.1089/adt.2019.940. Epub 2019 Sep 6.
Prostate cancer is the leading cause of cancer and second leading cause of cancer-related death in men in the United States. Twenty percent of patients receiving the standard of care androgen deprivation therapy (ADT) eventually progress to metastatic and incurable castration-resistant prostate cancer (CRPC). Current FDA-approved drugs for CRPC target androgen receptor (AR) binding or androgen production, but only provide a 2- to 5-month survival benefit due to the emergence of resistance. Overexpression of AR coactivators and the emergence of AR splice variants, both promote continued transcriptional activation under androgen-depleted conditions and represent drug resistance mechanisms that contribute to CRPC progression. The AR contains two transactivation domains, activation function 2 (AF-2) and activation function 1 (AF-1), which serve as binding surfaces for coactivators involved in the transcriptional activation of AR target genes. Full-length AR contains both AF-2 and AF-1 surfaces, whereas AR splice variants only have an AF-1 surface. We have recently prosecuted a high-content screening campaign to identify hit compounds that can inhibit or disrupt the protein-protein interactions (PPIs) between AR and transcriptional intermediary factor 2 (TIF2), one of the coactivators implicated in CRPC disease progression. Since an ideal inhibitor/disruptor of AR-coactivator PPIs would target both the AF-2 and AF-1 surfaces, we describe here the development and validation of five AF-2- and three AF-1-focused assays to interrogate and prioritize hits that disrupt both transactivation surfaces. The assays were validated using a test set of seven known AR modulator compounds, including three AR antagonists and one androgen synthesis inhibitor that are FDA-approved ADTs, two investigational molecules that target the N-terminal domain of AR, and an inhibitor of the Hsp90 (heat shock protein) molecular chaperone.
前列腺癌是美国男性癌症的主要病因及癌症相关死亡的第二大原因。接受标准护理雄激素剥夺疗法(ADT)的患者中有20%最终会进展为转移性且无法治愈的去势抵抗性前列腺癌(CRPC)。目前美国食品药品监督管理局(FDA)批准用于CRPC的药物靶向雄激素受体(AR)结合或雄激素生成,但由于耐药性的出现,仅能提供2至5个月的生存益处。AR共激活因子的过表达和AR剪接变体的出现,均促进了雄激素缺乏条件下的持续转录激活,并代表了导致CRPC进展的耐药机制。AR包含两个反式激活结构域,即激活功能2(AF-2)和激活功能1(AF-1),它们作为参与AR靶基因转录激活的共激活因子的结合表面。全长AR包含AF-2和AF-1表面,而AR剪接变体仅具有AF-1表面。我们最近开展了一项高内涵筛选活动,以鉴定能够抑制或破坏AR与转录中介因子2(TIF2)之间蛋白质-蛋白质相互作用(PPI)的活性化合物,TIF2是一种与CRPC疾病进展相关的共激活因子。由于理想的AR-共激活因子PPI抑制剂/破坏剂将靶向AF-2和AF-1表面,我们在此描述了五种针对AF-2和三种针对AF-1的检测方法的开发和验证,以询问并优先选择破坏两个反式激活表面的活性化合物。使用一组七种已知的AR调节剂化合物对这些检测方法进行了验证,其中包括三种AR拮抗剂和一种雄激素合成抑制剂(均为FDA批准的ADT)、两种靶向AR N端结构域的研究性分子以及一种热休克蛋白90(Hsp90)分子伴侣抑制剂。