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准SWI/SNF ATPases可以降低神经母细胞细胞的可塑性

Man Xu¹, Jason J Hong¹, Xiyuan Zhang¹

¹Pediatric Oncology Branch, Center for Cancer Research, National Cancer Institute, Bethesda, MD, USA.

The EMBO journal

|August 22, 2024

概括

SWI/SNF染色体重塑剂驱动神经母细胞瘤 (NB) 的可塑性和耐治疗性. 通过降解剂向这些ATPase抑制了NB的生长,并通过抑制可塑性相关的基因程序来防止化疗耐药性.

科学领域:

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
染色体重塑染色体重塑的方法

背景情况:

神经母细胞瘤 (NB) 表现出瘤细胞异质性,影响治疗反应.
NB包括上腺和介质细胞亚型,其中介质细胞特征在化疗后出现.
血统可塑性是NB亚型相互转换的基础,但机制尚不清楚.

研究的目的:

调查SWI/SNF染色体重塑复杂ATPases在NB谱系可塑性中的作用.
评估针对神经母细胞瘤中的SWI/SNF ATPases的治疗潜力.

主要方法:

使用SMARCA2/4双降解剂来准SWI/SNF ATPases.
对NB细胞增殖,入侵和细胞可塑性的评估影响.
分析了染色质可访问性,增强剂活性和转录因子结合.

主要成果:

SWI/SNF ATPases对于在上腺体NB中建立一个介酶基因允许性染色质状态至关重要.
用降解剂准SWI/SNF ATPases抑制了NB的扩散,入侵和可塑性.
SWI / SNF ATPase 枯竭导致染色质紧缩,增强剂活性降低,并取代了关键转录因子.

结论:

SWI/SNF ATPases是神经母细胞瘤内在可塑性和治疗耐药性的关键驱动因素.
向SWI/SNF ATPases代表了神经母细胞瘤组合治疗的有希望的表观遗传策略.

关键词:

癌细胞可塑性癌细胞可塑性核心转录因子核心转录因子表观遗传的可塑性表观遗传的可塑性神经母细胞瘤是一种神经母细胞瘤.在SWI/SNF复合体中.

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