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SWI/SNF nucleosome remodellers and cancer

SWI/SNF nucleosome remodellers and cancer Specific inactivating mutations in subunits of SWI/SNF chromatin remodelling complexes, including the SNF5 (also known as SMARCB1, INI1 and BAF47), ARID1A (also known as BAF250A and SMARCF1), BAF180 (also known as PBRM1) and BRM/SWI2-related gene 1 (BRG1; also known as SMARCA4) subunits, occur at a high frequency in several types of cancer. Genetically engineered mice carrying mutations in Snf5 and Brg1 have established that at least some SWI/SNF subunits have bona fide tumour suppressor activity. SWI/SNF complexes regulate gene expression by using the energy of ATP to remodel chromatin. A central function of SWI/SNF complexes is the coordinated regulation of gene expression programmes. These complexes have essential roles during lineage specification and in the maintenance of stem cell pluripotency. Emerging evidence has identified key pathways that contribute to tumorigenesis following perturbation of SWI/SNF complexes. Collectively, enzymes that modify chromatin structure are emerging as key regulators of tumorigenesis. As epigenetic alterations are potentially reversible, unlike DNA mutations, the targeted inhibition of chromatin-modifying enzymes may have important therapeutic implications for cancer. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Nature Reviews Cancer Springer Journals

SWI/SNF nucleosome remodellers and cancer

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References (143)

Publisher
Springer Journals
Copyright
Copyright © 2011 by Nature Publishing Group, a division of Macmillan Publishers Limited. All Rights Reserved.
Subject
Biomedicine; Biomedicine, general; Cancer Research
ISSN
1474-175X
eISSN
1474-1768
DOI
10.1038/nrc3068
Publisher site
See Article on Publisher Site

Abstract

Specific inactivating mutations in subunits of SWI/SNF chromatin remodelling complexes, including the SNF5 (also known as SMARCB1, INI1 and BAF47), ARID1A (also known as BAF250A and SMARCF1), BAF180 (also known as PBRM1) and BRM/SWI2-related gene 1 (BRG1; also known as SMARCA4) subunits, occur at a high frequency in several types of cancer. Genetically engineered mice carrying mutations in Snf5 and Brg1 have established that at least some SWI/SNF subunits have bona fide tumour suppressor activity. SWI/SNF complexes regulate gene expression by using the energy of ATP to remodel chromatin. A central function of SWI/SNF complexes is the coordinated regulation of gene expression programmes. These complexes have essential roles during lineage specification and in the maintenance of stem cell pluripotency. Emerging evidence has identified key pathways that contribute to tumorigenesis following perturbation of SWI/SNF complexes. Collectively, enzymes that modify chromatin structure are emerging as key regulators of tumorigenesis. As epigenetic alterations are potentially reversible, unlike DNA mutations, the targeted inhibition of chromatin-modifying enzymes may have important therapeutic implications for cancer.

Journal

Nature Reviews Cancer – Springer Journals

Published: Jun 9, 2011

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