Journal
CANCER LETTERS
Volume 419, Issue -, Pages 266-279Publisher
ELSEVIER IRELAND LTD
DOI: 10.1016/j.canlet.2018.01.046
Keywords
SWI/SNF complex; BAF complex; Chromatin assembly and disassembly; SWI/SNF-deficient pathology; BAF-deficient pathology
Categories
Funding
- Institut National de la Sante et de la Recherche Medicale
- Centre Leon Berard
- Cancer Research Center of Lyon
- Canceropole Ile de France
- Institut National du Cancer [INCa-PLBIO16-208]
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To activate or repress specific genes, chromatin is constantly modified by chromatin-remodeling complexes. Among these complexes, the SWItch/Sucrose Non-Fermenting (SWI/SNF) complex, also referred to as BRG1-Associated Factor (BAF) complex, moves the nucleosome along chromatin using energy provided by ATP hydrolysis. In mammalian organisms, the SWI/SNF complex is composed of 10-15 subunits, depending on cell type, and a defect in one of these subunits can have dramatic consequences. In this review we will focus on the alterations identified in the SWI/SNF (BAF) complex subunits that lead to cancerous pathologies. While SMARCB1 was the first mutated subunit to be reported in a majority of malignant rhabdoid tumors, the advent of next-generation sequencing allowed the discovery of mutations in various SWI/SNF subunits within a broad spectrum of cancers. In most cases, the mutation leads to a loss of expression or to a truncated subunit unable to perform its function. Even though it is now commonly acknowledged that approximately 20% of all cancers present a mutation in a SWI/SNF subunit, some cancers are associated to a specific alteration of a SWI/SNF subunit, which acts either as tumor suppressor genes or as oncogenes, and therefore constitute diagnostic or prognostic biomarkers. Consistently, therapeutic strategies targeting SWI/SNF subunits or the genes affected downstream have been revealed to treat cancers. (C) 2018 Elsevier B.V. All rights reserved.
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