hdac驱动的抗肿瘤机制:表观遗传学及其他。

IF 4.6 Q1 ONCOLOGY
癌症耐药(英文) Pub Date : 2024-11-20 eCollection Date: 2024-01-01 DOI:10.20517/cdr.2024.103
Martina Minisini, Martina Mascaro, Claudio Brancolini
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引用次数: 0

摘要

耐药的出现导致癌症复发是癌症患者治疗面临的挑战之一。几种机制可导致耐药性,包括表观遗传变化。组蛋白去乙酰化酶(hdac)通过表观遗传机制在染色质调控中发挥关键作用,也参与耐药性。组蛋白乙酰化的控制和调控DNA序列(如启动子、增强子和超级增强子)的可及性是hdac影响基因表达的已知机制。hdac的其他非组蛋白靶点也可能导致耐药性。这篇综述描述了hdac在某些情况下可能决定化疗或其他癌症治疗耐药的机制中的作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
HDAC-driven mechanisms in anticancer resistance: epigenetics and beyond.

The emergence of drug resistance leading to cancer recurrence is one of the challenges in the treatment of cancer patients. Several mechanisms can lead to drug resistance, including epigenetic changes. Histone deacetylases (HDACs) play a key role in chromatin regulation through epigenetic mechanisms and are also involved in drug resistance. The control of histone acetylation and the accessibility of regulatory DNA sequences such as promoters, enhancers, and super-enhancers are known mechanisms by which HDACs influence gene expression. Other targets of HDACs that are not histones can also contribute to resistance. This review describes the contribution of HDACs to the mechanisms that, in some cases, may determine resistance to chemotherapy or other cancer treatments.

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