ARD1/NAA10 acetylation in prostate cancer.
ARD1/NAA10 acetylation in prostate cancer.
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DOI：
10.1038/s12276-018-0107-0
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发表时间：
2018-07-27
影响因子：
12.8
通讯作者：
Liu W
中科院分区：
文献类型：
--
作者：
Kuhns KJ;Zhang G;Wang Z;Liu W
前列腺癌（PCa）是男性第二常见的癌症。雄激素受体（AR）信号通路在前列腺发育和体内平衡中发挥着至关重要的作用。该通路的失调会激活 AR，导致 PCa 发病和进展。 AR 结合睾酮和其他雄性激素，然后进行 AR 核转位和转录激活的翻译后修饰。因此，通过翻译后修饰激活 AR 对于 PCa 细胞的生长和存活至关重要。识别和理解 AR 修饰的病理和机制作用可能会增加我们对 PCa 中 AR 激活的理解，并提供新的治疗选择。最近，AR乙酰化被描述为AR激活的重要步骤。据报道，几种乙酰转移酶的上调与 PCa 进展相关。在此，我们提供对 AR 乙酰化的一般了解，特别强调 ARD1，以及可用于针对 ARD1-AR 轴进行 PCa 治疗的潜在疗法。通过 Arrest-defect-1 蛋白 (ARD1) 阻断雄激素受体上乙酰基的添加可能是阻止前列腺癌进展的有效策略。许多类型的癌症中都存在高水平的 ARD1，之前的研究表明，它通过刺激雄激素受体活性，有助于前列腺癌 (PCa) 细胞的增殖和存活。美国新奥尔良路易斯安那州立大学健康科学中心的 Wanguo Liu 及其同事回顾了 ARD1 对肿瘤形成的调节和影响的最新知识。 ARD1 介导的雄激素受体翻译后修饰使它们从细胞质移动到细胞核，并在细胞核中激活与肿瘤生长相关的基因的表达。抑制这种修饰的化合物可以为前列腺癌患者提供新的治疗选择。
Prostate cancer (PCa) is the second most common cancer in men. Androgen receptor (AR) signaling pathway plays a crucial role in prostate development and homeostasis. Dysregulation of this pathway activates AR leading to PCa pathogenesis and progression. AR binds testosterone and other male hormones, which then undergoes post-translational modification for AR nuclear translocation and transcriptional activation. AR activation by post-translational modification is thus imperative for PCa cell growth and survival. Identification and understanding of the pathological and mechanistic roles of AR modifications may increase our understanding of AR activation in PCa and provide new therapeutic options. Recently, AR acetylation has been described as an important step for AR activation. Upregulation of several acetyltransferases has been reported to be associated with PCa progression. Herein, we provide a general understanding of AR acetylation, with a special emphasis on ARD1, and potential therapies that may be exploited against the ARD1–AR axis for PCa treatment. Blocking the addition of an acetyl group to androgen receptors by Arrest-defect-1 protein (ARD1) might be an effective strategy for halting prostate cancer progression. High levels of ARD1 are found in many types of cancer and previous studies have shown that it contributes to prostate cancer (PCa) cell proliferation and survival by stimulating androgen receptor activity. Wanguo Liu and colleagues at Louisiana State University Health Sciences Center, New Orleans, USA, review current knowledge of the regulation and effects of ARD1 on tumor formation. The ARD1-mediated post-translational modification of androgen receptors causes them to move from the cytoplasm to the nucleus where they activate the expression of genes involved in tumor growth. Compounds that inhibit this modification could offer a new treatment option for patients with prostate cancer.
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影响因子：
4.8
作者：
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通讯作者：
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影响因子：
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作者：
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DOI：
10.1016/j.bbrc.2009.08.127
发表时间：
2009-11-06
影响因子：
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通讯作者：
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作者：
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影响因子：
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通讯作者：
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