Dihydrotestosterone(DHT) is an endogenous androgenic steroid and hormone that acts as an agonist for androgen receptors.
Dihydrotestosterone regulation of miRNA expression. CD44 expression and cell adhesion to hyaluronic acid (HA) were down-regulated when cells were treated with Dihydrotestosterone or transfection with a miR-328-3p mimic[1]. Altered miRNA levels when luminal breast cancer MCF-7 cancer cancer cells were treated with Dihydrotestosterone [2]. The expression of one critical miRNA, namely let-7a-d, was also found to be up-regulated in Dihydrotestosterone-treated MDA-MB-453 cells [3]. Treatment of MDA-MB-453 cells with Dihydrotestosterone causes down-regulation of miR-125b and miR-100 in association of increased expression of matrix metalloprotease 13, a target of both miRNAs [4]. Dihydrotestosterone treatment enhanced STAT5 phosphorylation and promoted proliferation of all CRPC cells. On immunofluorescence, activation of STAT5 and GR translocating into the nucleus after Dihydrotestosterone treatment [5].
Dihydrotestosterone induced early hair regression, hair miniaturization, hair density loss, and changes in hair morphology in male C57BL/6 mice [6]. The presence of the possible negative regulation of cell proliferation by Dihydrotestosterone. Moreover, cell proliferation related to urethral tube formation was revealed to be Dihydrotestosterone dose dependent [7]. Dihydrotestosterone-treated ovariectomized mice had free access to food (free-feeding), they had increased food intake and higher body weight compared with control animals. These mice also had a significantly greater accumulation of fat in the liver and exhibited increased fasting glucose, impaired glucose tolerance, and resistance to leptin [8]. Promastigotes in the presence of Dihydrotestosterone produced significantly larger lesions in BALB/c earlobes [9].
References:
[1]. Al-Othman N, Hammad H, et,al.Dihydrotestosterone regulates expression of CD44 via miR-328-3p in triple-negative breast cancer cells. Gene. 2018 Oct 30;675:128-135. doi: 10.1016/j.gene.2018.06.094. Epub 2018 Jun 28. PMID: 29964098.
[2]. Nakano K, Miki Y, et,al. Identification of androgen-responsive microRNAs and androgen-related genes in breast cancer. Anticancer Res. 2013 Nov;33(11):4811-9. PMID: 24222117.
[3]. Lyu S, Yu Q, et,al. Androgen receptor decreases CMYC and KRAS expression by upregulating let-7a expression in ER-, PR-, AR+ breast cancer. Int J Oncol. 2014 Jan;44(1):229-37. doi: 10.3892/ijo.2013.2151. Epub 2013 Oct 25. PMID: 24172884.
[4]. Ahram M, Mustafa E, et,al.Differential expression and androgen regulation of microRNAs and metalloprotease 13 in breast cancer cells. Cell Biol Int. 2017 Dec;41(12):1345-1355. doi: 10.1002/cbin.10841. Epub 2017 Sep 5. PMID: 28816390.
[5]. Song C, Kim Y, et,al. Dihydrotestosterone enhances castration-resistant prostate cancer cell proliferation through STAT5 activation via glucocorticoid receptor pathway. Prostate. 2014 Sep;74(12):1240-8. doi: 10.1002/pros.22841. Epub 2014 Jul 7. PMID: 25043756.
[6]. Fu D, Huang J, et,al. Dihydrotestosterone-induced hair regrowth inhibition by activating androgen receptor in C57BL6 mice simulates androgenetic alopecia. Biomed Pharmacother. 2021 May;137:111247. doi: 10.1016/j.biopha.2021.111247. Epub 2021 Jan 29. PMID: 33517191.
[7]. Suzuki H, Matsushita S, et,al. 5α-Dihydrotestosterone negatively regulates cell proliferation of the periurethral ventral mesenchyme during urethral tube formation in the murine male genital tubercle. Andrology. 2017 Jan;5(1):146-152. doi: 10.1111/andr.12241. Epub 2016 Oct 1. PMID: 27696776.
[8]. Kanaya N, Vonderfecht S, et,al. Androgen (dihydrotestosterone)-mediated regulation of food intake and obesity in female mice. J Steroid Biochem Mol Biol. 2013 Nov;138:100-6. doi: 10.1016/j.jsbmb.2013.04.001. Epub 2013 May 7. PMID: 23665441; PMCID: PMC4130703.
[9]. SÁnchez-GarcÍa L, Wilkins-Rodriguez A, et,al. Dihydrotestosterone enhances growth and infectivity of Leishmania Mexicana. Parasite Immunol. 2018 Mar;40(3). doi: 10.1111/pim.12512. Epub 2018 Jan 18. PMID: 29272044.
二氢睾酮 (DHT) 是一种内源性雄激素类固醇和激素,可作为雄激素受体的激动剂。
二氢睾酮对 miRNA 表达的调节。当用二氢睾酮处理细胞或用 miR-328-3p 模拟物转染细胞时,CD44 表达和细胞与透明质酸 (HA) 的粘附下调[1]。当用二氢睾酮[2] 处理管腔乳腺癌 MCF-7 癌细胞时,miRNA 水平发生了变化。还发现一种关键 miRNA,即 let-7a-d 的表达在二氢睾酮处理的 MDA-MB-453 细胞中上调 [3]。用二氢睾酮处理 MDA-MB-453 细胞会导致 miR-125b 和 miR-100 下调,这与基质金属蛋白酶 13 的表达增加有关,基质金属蛋白酶 13 是两种 miRNA 的靶标[4]。双氢睾酮治疗增强了 STAT5 磷酸化并促进了所有 CRPC 细胞的增殖。免疫荧光显示,双氢睾酮处理后 STAT5 激活和 GR 易位入核[5]。
双氢睾酮诱导早期毛发退化、毛发小型化、毛发密度下降和毛发变化雄性 C57BL/6 小鼠的形态 [6]。二氢睾酮可能存在对细胞增殖的负调节。此外,与尿道管形成相关的细胞增殖显示为二氢睾酮剂量依赖性[7]。双氢睾酮治疗的卵巢切除小鼠可以自由进食（自由喂养）,与对照动物相比,它们的食物摄入量增加,体重增加。这些小鼠在肝脏中的脂肪堆积也明显增加,并表现出空腹血糖升高、葡萄糖耐量降低和瘦素抵抗[8]。双氢睾酮存在下的前鞭毛体在 BALB/c 耳垂中产生了明显更大的损伤 [9]。