开放与变化:哺乳动物器官发育和癌变过程中的 SWI/SNF 复合物。

IF 4.5 3区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY
Open Biology Pub Date : 2024-10-01 Epub Date: 2024-10-30 DOI:10.1098/rsob.240039
Fadia Abu Sailik, Bright Starling Emerald, Suraiya Anjum Ansari
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引用次数: 0

摘要

开关/蔗糖不发酵(SWI/SNF)亚家族是进化保守的、依赖 ATP 的染色质重塑复合物,可改变核小体的位置并调控一系列核过程,包括基因表达、DNA 复制、DNA 损伤修复、基因组稳定性和肿瘤抑制。这些复合物通过其 ATP 依赖性染色质重塑作用,对遗传信息的动态调控以及对正常细胞功能和整体基因组完整性至关重要的细胞过程的维持做出了贡献。在 25% 的人类恶性肿瘤中都能检测到 SWI/SNF 亚基的突变,这表明该复合体的高效运作是防止不同组织中肿瘤发生的必要条件。在发育过程中,SWI/SNF 亚基有助于建立和维持对正确的细胞特性和功能至关重要的基因表达模式,包括维持细胞系特异性增强子。此外,与 SWI/SNF 基因突变相关的特定分子特征,包括增强子上的 SWI/SNF 活性被破坏、G0 细胞周期停滞的逃避、通过促癌基因激活和多聚酶群 (PcG) 复合体拮抗诱导细胞可塑性,都与癌变的发生和发展有关。在此,我们回顾了对由 SWI/SNF 复合物破坏所导致的人类恶性肿瘤病因的分子认识,并将这些机制与它们的发育功能联系起来。最后,我们讨论了靶向 SWI/SNF 亚基治疗癌症的潜力。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Opening and changing: mammalian SWI/SNF complexes in organ development and carcinogenesis.

The switch/sucrose non-fermentable (SWI/SNF) subfamily are evolutionarily conserved, ATP-dependent chromatin-remodelling complexes that alter nucleosome position and regulate a spectrum of nuclear processes, including gene expression, DNA replication, DNA damage repair, genome stability and tumour suppression. These complexes, through their ATP-dependent chromatin remodelling, contribute to the dynamic regulation of genetic information and the maintenance of cellular processes essential for normal cellular function and overall genomic integrity. Mutations in SWI/SNF subunits are detected in 25% of human malignancies, indicating that efficient functioning of this complex is required to prevent tumourigenesis in diverse tissues. During development, SWI/SNF subunits help establish and maintain gene expression patterns essential for proper cellular identity and function, including maintenance of lineage-specific enhancers. Moreover, specific molecular signatures associated with SWI/SNF mutations, including disruption of SWI/SNF activity at enhancers, evasion of G0 cell cycle arrest, induction of cellular plasticity through pro-oncogene activation and Polycomb group (PcG) complex antagonism, are linked to the initiation and progression of carcinogenesis. Here, we review the molecular insights into the aetiology of human malignancies driven by disruption of the SWI/SNF complex and correlate these mechanisms to their developmental functions. Finally, we discuss the therapeutic potential of targeting SWI/SNF subunits in cancer.

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来源期刊
Open Biology
Open Biology BIOCHEMISTRY & MOLECULAR BIOLOGY-
CiteScore
10.00
自引率
1.70%
发文量
136
审稿时长
6-12 weeks
期刊介绍: Open Biology is an online journal that welcomes original, high impact research in cell and developmental biology, molecular and structural biology, biochemistry, neuroscience, immunology, microbiology and genetics.
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