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染色质重塑与癌症：SWI/SNF复合物的关键影响

Chromatin remodeling and cancer: the critical influence of the SWI/SNF complex.

作者信息

Hao Fengxiang, Zhang Ying, Hou Jiayi, Zhao Bin

机构信息

Shanxi Medical University, Taiyuan, Shanxi Province, 030001, China.

Shanxi Province Key Laboratory of Oral Diseases Prevention and New Materials, Shanxi Medical University School and Hospital of Stomatology, Taiyuan, Shanxi Province, 030001, China.

出版信息

Epigenetics Chromatin. 2025 Apr 23;18(1):22. doi: 10.1186/s13072-025-00590-w.

DOI:10.1186/s13072-025-00590-w
PMID:40269969
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12016160/
Abstract

The SWI/SNF complex was first identified in yeast and named after studies of mutants critical for the mating-type switch (SWI) and sucrose non-fermenting (SNF) pathways.The SWI/SNF complex plays a pivotal role in regulating gene expression by altering chromatin structure to promote or suppress the expression of specific genes, maintain stem cell pluripotency, and participate in various biological processes. Mutations in the SWI/SNF complex are highly prevalent in various human cancers, significantly impacting tumor suppressive or oncogenic functions and influencing tumor initiation and progression. This review focuses on the mechanisms by which ARID1A/ARID1B, PBRM1, SMARCB1, and SMARCA2/SMARCA4 contribute to cancer, the immunoregulatory roles of the SWI/SNF complex, its involvement in DNA repair pathways, synthetic lethality, and applications in precision oncology.

摘要

SWI/SNF复合物最初是在酵母中发现的，以对交配型转换（SWI）和蔗糖非发酵（SNF）途径至关重要的突变体研究而命名。SWI/SNF复合物通过改变染色质结构来促进或抑制特定基因的表达、维持干细胞多能性并参与各种生物学过程，在调节基因表达中起关键作用。SWI/SNF复合物的突变在各种人类癌症中高度普遍，显著影响肿瘤抑制或致癌功能，并影响肿瘤的发生和进展。本综述重点关注ARID1A/ARID1B、PBRM1、SMARCB1和SMARCA2/SMARCA4导致癌症的机制、SWI/SNF复合物的免疫调节作用、其在DNA修复途径中的参与、合成致死性以及在精准肿瘤学中的应用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9a89/12016160/cbc96f38b34e/13072_2025_590_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9a89/12016160/948bdc2f6bea/13072_2025_590_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9a89/12016160/2ce4d593c6e3/13072_2025_590_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9a89/12016160/cbc96f38b34e/13072_2025_590_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9a89/12016160/948bdc2f6bea/13072_2025_590_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9a89/12016160/2ce4d593c6e3/13072_2025_590_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9a89/12016160/cbc96f38b34e/13072_2025_590_Fig3_HTML.jpg

相似文献

[1]
Chromatin remodeling and cancer: the critical influence of the SWI/SNF complex.

Epigenetics Chromatin. 2025-4-23

[2]
Loss of the SWI/SNF-ATPase subunit members SMARCF1 (ARID1A), SMARCA2 (BRM), SMARCA4 (BRG1) and SMARCB1 (INI1) in oesophageal adenocarcinoma.

BMC Cancer. 2020-1-6

[3]
Update on SWI/SNF-related gynecologic mesenchymal neoplasms: SMARCA4-deficient uterine sarcoma and SMARCB1-deficient vulvar neoplasms.

Genes Chromosomes Cancer. 2021-3

[4]
BAFfling pathologies: Alterations of BAF complexes in cancer.

Cancer Lett. 2018-1-31

[5]
SWI/SNF complex in cancer.

Nat Genet. 2017-1-31

[6]
Frequent co-inactivation of the SWI/SNF subunits SMARCB1, SMARCA2 and PBRM1 in malignant rhabdoid tumours.

Histopathology. 2015-2-5

[7]
Inactivating mutations in SWI/SNF chromatin remodeling genes in human cancer.

Jpn J Clin Oncol. 2013-7-30

[8]
Dual loss of the SWI/SNF complex ATPases SMARCA4/BRG1 and SMARCA2/BRM is highly sensitive and specific for small cell carcinoma of the ovary, hypercalcaemic type.

J Pathol. 2016-2

[9]
[Chromatin remodeling defects and cancer: the SWI/SNF example].

Bull Cancer. 2012-12

[10]
SWI/SNF Complex-deficient Undifferentiated/Rhabdoid Carcinomas of the Gastrointestinal Tract: A Series of 13 Cases Highlighting Mutually Exclusive Loss of SMARCA4 and SMARCA2 and Frequent Co-inactivation of SMARCB1 and SMARCA2.

Am J Surg Pathol. 2016-4

引用本文的文献

[1]
SMARCB1-related schwannomatosis and other SMARCB1-associated phenotypes: clinical spectrum and molecular pathogenesis.

Fam Cancer. 2025-8-12

本文引用的文献

[1]
Discovery of FHD-286, a First-in-Class, Orally Bioavailable, Allosteric Dual Inhibitor of the Brahma Homologue (BRM) and Brahma-Related Gene 1 (BRG1) ATPase Activity for the Treatment of SWItch/Sucrose Non-Fermentable (SWI/SNF) Dependent Cancers.

J Med Chem. 2025-1-23

[2]
Enhancer reprogramming underlies therapeutic utility of a SMARCA2 degrader in SMARCA4 mutant cancer.

Cell Chem Biol. 2024-12-19

[3]
Hepatocellular carcinoma-specific epigenetic checkpoints bidirectionally regulate the antitumor immunity of CD4 + T cells.

Cell Mol Immunol. 2024-11

[4]
Chromatin remodellers as therapeutic targets.

Nat Rev Drug Discov. 2024-9

[5]
SETMAR Facilitates the Differentiation of Thyroid Cancer by Regulating SMARCA2-Mediated Chromatin Remodeling.

Adv Sci (Weinh). 2024-8

[6]
Collaboration between distinct SWI/SNF chromatin remodeling complexes directs enhancer selection and activation of macrophage inflammatory genes.

Immunity. 2024-8-13

[7]
Targeting dependency on a paralog pair of CBP/p300 against de-repression of KREMEN2 in SMARCB1-deficient cancers.

Nat Commun. 2024-6-5

[8]
ARID1A loss promotes RNA editing of CDK13 in an ADAR1-dependent manner.

BMC Biol. 2024-6-5

[9]
Therapeutic targeting of ARID1A-deficient cancer cells with RITA (Reactivating p53 and inducing tumor apoptosis).

Cell Death Dis. 2024-5-29

[10]
Molecular characteristics of early-onset compared with late-onset colorectal cancer: a case controlled study.

Int J Surg. 2024-8-1

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