Advances in the study of the role of high-frequency mutant subunits of the SWI/SNF complex in tumors

SWI/SNF (Switch/Sucrose non-fermentable, switch/sucrose non-fermentable) chromatin remodeling complex is a macromolecular complex composed of multiple subunits. It can use the energy generated by the hydrolysis of ATP (Adenosine triphosphate) to destroy the connection between DNA and histones, achie...

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Main Authors: Jiumei Zhao, Jing Zhu, Yu Tang, Kepu Zheng, Ziwei Li
Format: Article
Language:English
Published: Frontiers Media S.A. 2024-12-01
Series:Frontiers in Oncology
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Online Access:https://www.frontiersin.org/articles/10.3389/fonc.2024.1463892/full
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author Jiumei Zhao
Jing Zhu
Yu Tang
Kepu Zheng
Ziwei Li
author_facet Jiumei Zhao
Jing Zhu
Yu Tang
Kepu Zheng
Ziwei Li
author_sort Jiumei Zhao
collection DOAJ
description SWI/SNF (Switch/Sucrose non-fermentable, switch/sucrose non-fermentable) chromatin remodeling complex is a macromolecular complex composed of multiple subunits. It can use the energy generated by the hydrolysis of ATP (Adenosine triphosphate) to destroy the connection between DNA and histones, achieve the breakdown of nucleosomes, and regulate gene expression. SWI/SNF complex is essential for cell proliferation and differentiation, and the abnormal function of its subunits is closely related to tumorigenesis. Among them, ARID1A, an essential non-catalytic subunit of the SWI/SNF complex, can regulate the targeting of the complex through DNA or protein interactions. Moreover, the abnormal function of ARID1A significantly reduces the targeting of SWI/SNF complex to genes and participates in critical intracellular activities such as gene transcription and DNA synthesis. As a catalytic subunit of the SWI/SNF complex, SMARCA4 has ATPase activity that catalyzes the hydrolysis of ATP to produce energy and power the chromatin remodeling complex, which is critical to the function of the SWI/SNF complex. The study data indicate that approximately 25% of cancers have one or more SWI/SNF subunit genetic abnormalities, and at least nine different SWI/SNF subunits have been identified as having repeated mutations multiple times in various cancers, suggesting that mutations affecting SWI/SNF subunits may introduce vulnerabilities to these cancers. Here, we review the mechanism of action of ARID1A and SMARCA4, the two subunits with the highest mutation frequency in the SWI/SNF complex, and the research progress of their targeted therapy in tumors to provide a new direction for precise targeted therapy of clinical tumors.
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spelling doaj-art-7d4d8a5258ab488bb3113afa4011b3a82025-08-20T02:19:54ZengFrontiers Media S.A.Frontiers in Oncology2234-943X2024-12-011410.3389/fonc.2024.14638921463892Advances in the study of the role of high-frequency mutant subunits of the SWI/SNF complex in tumorsJiumei Zhao0Jing Zhu1Yu Tang2Kepu Zheng3Ziwei Li4Chongqing Nanchuan District People’s Hospital, Chongqing, ChinaKunming Medical University, Kunming, ChinaThe Third Affiliated Hospital of Kunming Medical University, Kunming, ChinaKunming Medical University, Kunming, ChinaChongqing Health Center for Women and Children, Women and Children’s Hospital of Chongqing Medical University, Chongqing, ChinaSWI/SNF (Switch/Sucrose non-fermentable, switch/sucrose non-fermentable) chromatin remodeling complex is a macromolecular complex composed of multiple subunits. It can use the energy generated by the hydrolysis of ATP (Adenosine triphosphate) to destroy the connection between DNA and histones, achieve the breakdown of nucleosomes, and regulate gene expression. SWI/SNF complex is essential for cell proliferation and differentiation, and the abnormal function of its subunits is closely related to tumorigenesis. Among them, ARID1A, an essential non-catalytic subunit of the SWI/SNF complex, can regulate the targeting of the complex through DNA or protein interactions. Moreover, the abnormal function of ARID1A significantly reduces the targeting of SWI/SNF complex to genes and participates in critical intracellular activities such as gene transcription and DNA synthesis. As a catalytic subunit of the SWI/SNF complex, SMARCA4 has ATPase activity that catalyzes the hydrolysis of ATP to produce energy and power the chromatin remodeling complex, which is critical to the function of the SWI/SNF complex. The study data indicate that approximately 25% of cancers have one or more SWI/SNF subunit genetic abnormalities, and at least nine different SWI/SNF subunits have been identified as having repeated mutations multiple times in various cancers, suggesting that mutations affecting SWI/SNF subunits may introduce vulnerabilities to these cancers. Here, we review the mechanism of action of ARID1A and SMARCA4, the two subunits with the highest mutation frequency in the SWI/SNF complex, and the research progress of their targeted therapy in tumors to provide a new direction for precise targeted therapy of clinical tumors.https://www.frontiersin.org/articles/10.3389/fonc.2024.1463892/fullSWI/SNF complexARID1ASMARCA4tumortumor resistancemolecular mechanism
spellingShingle Jiumei Zhao
Jing Zhu
Yu Tang
Kepu Zheng
Ziwei Li
Advances in the study of the role of high-frequency mutant subunits of the SWI/SNF complex in tumors
Frontiers in Oncology
SWI/SNF complex
ARID1A
SMARCA4
tumor
tumor resistance
molecular mechanism
title Advances in the study of the role of high-frequency mutant subunits of the SWI/SNF complex in tumors
title_full Advances in the study of the role of high-frequency mutant subunits of the SWI/SNF complex in tumors
title_fullStr Advances in the study of the role of high-frequency mutant subunits of the SWI/SNF complex in tumors
title_full_unstemmed Advances in the study of the role of high-frequency mutant subunits of the SWI/SNF complex in tumors
title_short Advances in the study of the role of high-frequency mutant subunits of the SWI/SNF complex in tumors
title_sort advances in the study of the role of high frequency mutant subunits of the swi snf complex in tumors
topic SWI/SNF complex
ARID1A
SMARCA4
tumor
tumor resistance
molecular mechanism
url https://www.frontiersin.org/articles/10.3389/fonc.2024.1463892/full
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