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HDAC是改善瘤放射治疗耐药性的重要标

Rui Ling¹, Jingzhi Wang², Yuan Fang¹

¹Department of Oncology, Affiliated Hospital of Jiangsu University, Zhenjiang, China.

Frontiers in oncology

|July 28, 2023

概括

基因组脱乙酶 (HDACs) 通过影响DNA修复和细胞存活来驱动瘤放射治疗耐药性. 用抑制剂向HDAC可能会提高癌症治疗的疗效.

科学领域:

在瘤学瘤学.
表观遗传学在表观遗传学中,表观遗传学是指表观遗传学.
癌症生物学癌症生物学

背景情况:

放射治疗是癌症治疗的基石,但耐药性仍然是一个重大的临床挑战.
放射治疗耐药性的机制包括DNA修复,细胞循环和表观遗传修饰.
基因组脱乙酶 (HDACs) 是关键的表观遗传调节剂,涉及各种癌症过程.

研究的目的:

系统地阐明HDACs促进瘤放射治疗耐药性的机制.
探索HDAC抑制剂在克服放射治疗耐药性的临床应用前景.
为与HDAC相关的药物开发和未来研究方向提供参考.

主要方法:

对HDACs和放射治疗耐药性的现有文献进行审查和综合.
在体内和体外研究的分析,详细说明HDAC参与抗性机制.
检查表观遗传修饰在细胞对辐射反应中的作用.

主要成果:

HDACs通过多种机制促进放射治疗耐药性,包括DNA损伤修复,细胞循环调节和亡调节.
由HDACs调节的表观遗传变化对于治疗耐药性的发展至关重要.
在临床前模型中,HDAC 抑制剂在提高放射治疗疗效方面表现有前途.

结论:

HDACs在通过表观遗传调节促进瘤放射治疗耐药性方面发挥着至关重要的作用.
HDAC 抑制剂代表了一种有前途的治疗策略,以克服放射治疗耐药性.
对HDAC及其抑制剂的进一步研究是有必要的,以改善癌症治疗结果.

关键词:

DSBR 是一个 DSBR 系统.HDAC 抑制剂的使用这就是HDACs.细胞循环中的细胞循环.抗辐射疗法耐药性抗辐射治疗耐药性

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