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组蛋白去乙酰化酶驱动的抗癌耐药机制:表观遗传学及其他。

HDAC-driven mechanisms in anticancer resistance: epigenetics and beyond.

作者信息

Minisini Martina, Mascaro Martina, Brancolini Claudio

机构信息

Laboratory of Epigenomics, Department of Medicine, Università degli Studi di Udine, Udine 33100, Italy.

出版信息

Cancer Drug Resist. 2024 Nov 20;7:46. doi: 10.20517/cdr.2024.103. eCollection 2024.

Abstract

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.

摘要

导致癌症复发的耐药性的出现是癌症患者治疗中的挑战之一。多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(HDACs)通过表观遗传机制在染色质调控中发挥关键作用,并且也参与耐药性。组蛋白乙酰化的控制以及诸如启动子、增强子和超级增强子等调控DNA序列的可及性是HDACs影响基因表达的已知机制。HDACs的非组蛋白其他靶点也可能导致耐药性。本综述描述了HDACs在某些情况下可能决定对化疗或其他癌症治疗耐药性的机制中的作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2192/11609180/1f7ed8421755/cdr-7-46.fig.1.jpg

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