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癌蛋白转录因子 MYC 与 SWI/SNF 染色质重塑因子的多种相互作用。

Multiple interactions of the oncoprotein transcription factor MYC with the SWI/SNF chromatin remodeler.

机构信息

Department of Cell and Developmental Biology, Vanderbilt University School of Medicine, Nashville, TN, USA.

Department of Biology, Middle Tennessee State University, Murfreesboro, TN, USA.

出版信息

Oncogene. 2021 May;40(20):3593-3609. doi: 10.1038/s41388-021-01804-7. Epub 2021 Apr 30.

DOI:10.1038/s41388-021-01804-7
PMID:33931740
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8141032/
Abstract

The SNF5 subunit of the SWI/SNF chromatin remodeling complex has been shown to act as a tumor suppressor through multiple mechanisms, including impairing the ability of the oncoprotein transcription factor MYC to bind chromatin. Beyond SNF5, however, it is unknown to what extent MYC can access additional SWI/SNF subunits or how these interactions affect the ability of MYC to drive transcription, particularly in SNF5-null cancers. Here, we report that MYC interacts with multiple SWI/SNF components independent of SNF5. We show that MYC binds the pan-SWI/SNF subunit BAF155 through the BAF155 SWIRM domain, an interaction that is inhibited by the presence of SNF5. In SNF5-null cells, MYC binds with remaining SWI/SNF components to essential genes, although for a purpose that is distinct from chromatin remodeling. Analysis of MYC-SWI/SNF target genes in SNF5-null cells reveals that they are associated with core biological functions of MYC linked to protein synthesis. These data reveal that MYC can bind SWI/SNF in an SNF5-independent manner and that SNF5 modulates access of MYC to core SWI/SNF complexes. This work provides a framework in which to interrogate the influence of SWI/SNF on MYC function in cancers in which SWI/SNF or MYC are altered.

摘要

SWI/SNF 染色质重塑复合物的 SNF5 亚基已被证明通过多种机制发挥肿瘤抑制因子的作用，包括削弱致癌蛋白转录因子 MYC 与染色质结合的能力。然而，除了 SNF5 之外，目前尚不清楚 MYC 能够在多大程度上接近其他 SWI/SNF 亚基，或者这些相互作用如何影响 MYC 驱动转录的能力，特别是在 SNF5 缺失的癌症中。在这里，我们报告 MYC 与多个 SWI/SNF 成分相互作用，而不依赖于 SNF5。我们表明，MYC 通过 BAF155 的 SWIRM 结构域与泛 SWI/SNF 亚基 BAF155 结合，这种相互作用被 SNF5 的存在所抑制。在 SNF5 缺失的细胞中，MYC 与剩余的 SWI/SNF 成分结合到必需基因上，尽管其结合目的与染色质重塑不同。对 SNF5 缺失细胞中 MYC-SWI/SNF 靶基因的分析表明，它们与 MYC 与蛋白质合成相关的核心生物学功能有关。这些数据表明，MYC 可以以不依赖于 SNF5 的方式与 SWI/SNF 结合，并且 SNF5 调节 MYC 接近核心 SWI/SNF 复合物的能力。这项工作为研究 SWI/SNF 在 SWI/SNF 或 MYC 改变的癌症中对 MYC 功能的影响提供了一个框架。

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