Gillen Andrew D, Hunter Irene, Ullner Ekkehard, McEwan Iain J
Institute of Medical Sciences, School of Medicine, Medical Sciences and Nutrition, University of Aberdeen, Scotland, United Kingdom.
Department of Physics, Institute of Complex Sciences and Mathematical Biology University of Aberdeen, Scotland, United Kingdom.
PLoS One. 2024 Aug 1;19(8):e0304183. doi: 10.1371/journal.pone.0304183. eCollection 2024.
Expression of the androgen receptor is key to the response of cells and tissues to androgenic steroids, such as testosterone or dihydrotestosterone, as well as impacting the benefit of hormone-dependent therapies for endocrine diseases and hormone-dependent cancers. However, the mechanisms controlling androgen receptor expression are not fully understood, limiting our ability to effectively promote or inhibit androgenic signalling therapeutically. An autoregulatory loop has been described in which androgen receptor may repress its own expression in the presence of hormone, although the molecular mechanisms are not fully understood. In this work, we elucidate the mechanisms of autoregulation and demonstrate, for the first time, that a similar repression of the AR gene is facilitated by the progesterone receptor. We show that the progesterone receptor, like the androgen receptor binds to response elements within the AR gene to effect transcriptional repression in response to hormone treatment. Mechanistically, this repression involves hormone-dependent histone deacetylation within the AR 5'UTR region and looping between sequences in intron 2 and the transcription start site (TSS). This novel pathway controlling AR expression in response to hormone stimulation may have important implications for understanding cell or tissue selective receptor signalling.
雄激素受体的表达是细胞和组织对雄激素类固醇(如睾酮或二氢睾酮)作出反应的关键,同时也影响着内分泌疾病和激素依赖性癌症的激素依赖性疗法的疗效。然而,控制雄激素受体表达的机制尚未完全明确,这限制了我们通过治疗手段有效促进或抑制雄激素信号传导的能力。虽然分子机制尚未完全清楚,但已有研究描述了一种自调节环路,即在激素存在的情况下,雄激素受体可能会抑制其自身的表达。在这项研究中,我们阐明了自调节机制,并首次证明孕激素受体会促进AR基因的类似抑制作用。我们发现,孕激素受体与雄激素受体一样,会结合到AR基因内的反应元件上,以响应激素处理从而实现转录抑制。从机制上讲,这种抑制涉及AR 5'UTR区域内激素依赖性组蛋白去乙酰化以及内含子2中的序列与转录起始位点(TSS)之间的环化。这种响应激素刺激控制AR表达的新途径可能对理解细胞或组织选择性受体信号传导具有重要意义。