前列腺癌进展中的表观遗传调控。

Current molecular biology reports Pub Date : 2018-01-01 Epub Date: 2018-04-18 DOI:10.1007/s40610-018-0095-9
Katia Ruggero, Sonia Farran-Matas, Adrian Martinez-Tebar, Alvaro Aytes
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引用次数: 41

摘要

综述目的:前列腺癌中一些重要的新发现的分子改变影响染色质生物学的主要调控基因编码和表观遗传调控。这篇综述将提供前列腺癌进展的关键表观遗传机制、治疗耐药、潜在的可操作机制和生物标志物的最新观点。最近的发现:染色质生物学和表观遗传主调控因子的关键参与者最近被描述为在转移性CRPC和进展为AR独立的肿瘤中发生关键改变。因此,当前列腺癌细胞失去ar强加的身份时,表观遗传失调代表了重编程的驱动机制。摘要:染色质完整性和转录调控的可及性是癌症进展中改变的关键特征,在核激素受体驱动的肿瘤(如前列腺癌)中尤为重要。了解染色质重塑如何决定前列腺的发育,以及染色质重塑如何影响前列腺癌的发生和发展,可能会改善前列腺癌患者的风险分层和治疗选择。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Epigenetic Regulation in Prostate Cancer Progression.

Purpose of review: An important number of newly identified molecular alterations in prostate cancer affect gene encoding master regulators of chromatin biology epigenetic regulation. This review will provide an updated view of the key epigenetic mechanisms underlying prostate cancer progression, therapy resistance, and potential actionable mechanisms and biomarkers.

Recent findings: Key players in chromatin biology and epigenetic master regulators has been recently described to be crucially altered in metastatic CRPC and tumors that progress to AR independency. As such, epigenetic dysregulation represents a driving mechanism in the reprograming of prostate cancer cells as they lose AR-imposed identity.

Summary: Chromatin integrity and accessibility for transcriptional regulation are key features altered in cancer progression, and particularly relevant in nuclear hormone receptor-driven tumors like prostate cancer. Understanding how chromatin remodeling dictates prostate development and how its deregulation contributes to prostate cancer onset and progression may improve risk stratification and treatment selection for prostate cancer patients.

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