Valentín López José C, Lange Carol A, Dehm Scott M
Masonic Cancer Center, University of Minnesota, Minneapolis, MN, USA.
Masonic Cancer Center, University of Minnesota, Minneapolis, MN, USA; Department of Medicine-Hematology, Oncology & Transplantation, University of Minnesota, Minneapolis, MN, USA.
J Steroid Biochem Mol Biol. 2024 Jul;241:106522. doi: 10.1016/j.jsbmb.2024.106522. Epub 2024 Apr 17.
The androgen receptor (AR) and estrogen receptor alpha (ERα) are steroid receptor transcription factors with critical roles in the development and progression of prostate and breast cancers. Advances in the understanding of mechanisms underlying the ligand-dependent activation of these transcription factors have contributed to the development of small molecule inhibitors that block AR and ERα actions. These inhibitors include competitive antagonists and degraders that directly bind the ligand binding domains of these receptors, luteinizing hormone releasing hormone (LHRH) analogs that suppress gonadal synthesis of testosterone or estrogen, and drugs that block specific enzymes required for biosynthesis of testosterone or estrogen. However, resistance to these therapies is frequent, and is often driven by selection for tumor cells with alterations in the AR or ESR1 genes and/or alternatively spliced AR or ESR1 mRNAs that encode variant forms AR or ERα. While most investigations involving AR have been within the context of prostate cancer, and the majority of investigations involving ERα have been within the context of breast cancer, important roles for AR have been elucidated in breast cancer, and important roles for ERα have been elucidated in prostate cancer. Here, we will discuss the roles of AR and ERα in breast and prostate cancers, outline the effects of gene- and mRNA-level alterations in AR and ESR1 on progression of these diseases, and identify strategies that are being developed to target these alterations therapeutically.
雄激素受体(AR)和雌激素受体α(ERα)是类固醇受体转录因子,在前列腺癌和乳腺癌的发生发展中起关键作用。对这些转录因子配体依赖性激活机制认识的进展,推动了阻断AR和ERα作用的小分子抑制剂的研发。这些抑制剂包括直接结合这些受体配体结合域的竞争性拮抗剂和降解剂、抑制睾酮或雌激素性腺合成的促黄体生成素释放激素(LHRH)类似物,以及阻断睾酮或雌激素生物合成所需特定酶的药物。然而,对这些疗法的耐药性很常见,且通常是由选择具有AR或ESR1基因改变和/或编码变异形式AR或ERα的选择性剪接AR或ESR1 mRNA的肿瘤细胞所驱动。虽然大多数涉及AR的研究是在前列腺癌背景下进行的,而大多数涉及ERα的研究是在乳腺癌背景下进行的,但AR在乳腺癌中的重要作用已得到阐明,ERα在前列腺癌中的重要作用也已得到阐明。在此,我们将讨论AR和ERα在乳腺癌和前列腺癌中的作用,概述AR和ESR1基因及mRNA水平改变对这些疾病进展的影响,并确定正在研发的针对这些改变进行治疗的策略。