The role of SWI/SNF chromatin remodelers in the repair of DNA double strand breaks and cancer therapy
Switch/Sucrose non-fermenting (SWI/SNF) chromatin remodelers hydrolyze ATP to push and slide nucleosomes along the DNA thus modulating access to various genomic loci. These complexes are the most frequently mutated epigenetic regulators in human cancers. SWI/SNF complexes are well known for their fu...
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| Format: | Article |
| Language: | English |
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Frontiers Media S.A.
2022-12-01
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| Series: | Frontiers in Cell and Developmental Biology |
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| Online Access: | https://www.frontiersin.org/articles/10.3389/fcell.2022.1071786/full |
| _version_ | 1828263753596010496 |
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| author | Maria Sadek Anand Sheth Grant Zimmerman Emily Hays Renier Vélez-Cruz Renier Vélez-Cruz Renier Vélez-Cruz Renier Vélez-Cruz |
| author_facet | Maria Sadek Anand Sheth Grant Zimmerman Emily Hays Renier Vélez-Cruz Renier Vélez-Cruz Renier Vélez-Cruz Renier Vélez-Cruz |
| author_sort | Maria Sadek |
| collection | DOAJ |
| description | Switch/Sucrose non-fermenting (SWI/SNF) chromatin remodelers hydrolyze ATP to push and slide nucleosomes along the DNA thus modulating access to various genomic loci. These complexes are the most frequently mutated epigenetic regulators in human cancers. SWI/SNF complexes are well known for their function in transcription regulation, but more recent work has uncovered a role for these complexes in the repair of DNA double strand breaks (DSBs). As radiotherapy and most chemotherapeutic agents kill cancer cells by inducing double strand breaks, by identifying a role for these complexes in double strand break repair we are also identifying a DNA repair vulnerability that can be exploited therapeutically in the treatment of SWI/SNF-mutated cancers. In this review we summarize work describing the function of various SWI/SNF subunits in the repair of double strand breaks with a focus on homologous recombination repair and discuss the implication for the treatment of cancers with SWI/SNF mutations. |
| first_indexed | 2024-04-13T04:15:18Z |
| format | Article |
| id | doaj.art-46e9bce1b685481c8580ea7dccddfd84 |
| institution | Directory Open Access Journal |
| issn | 2296-634X |
| language | English |
| last_indexed | 2024-04-13T04:15:18Z |
| publishDate | 2022-12-01 |
| publisher | Frontiers Media S.A. |
| record_format | Article |
| series | Frontiers in Cell and Developmental Biology |
| spelling | doaj.art-46e9bce1b685481c8580ea7dccddfd842022-12-22T03:02:59ZengFrontiers Media S.A.Frontiers in Cell and Developmental Biology2296-634X2022-12-011010.3389/fcell.2022.10717861071786The role of SWI/SNF chromatin remodelers in the repair of DNA double strand breaks and cancer therapyMaria Sadek0Anand Sheth1Grant Zimmerman2Emily Hays3Renier Vélez-Cruz4Renier Vélez-Cruz5Renier Vélez-Cruz6Renier Vélez-Cruz7Biomedical Sciences Program, College of Graduate Studies, Midwestern University, Downers Grove, IL, United StatesChicago College of Osteopathic Medicine, Midwestern University, Downers Grove, IL, United StatesChicago College of Osteopathic Medicine, Midwestern University, Downers Grove, IL, United StatesDepartment of Biochemistry and Molecular Genetics, College of Graduate Studies, Midwestern University, Downers Grove, IL, United StatesDepartment of Biochemistry and Molecular Genetics, College of Graduate Studies, Midwestern University, Downers Grove, IL, United StatesChicago College of Osteopathic Medicine, Midwestern University, Downers Grove, IL, United StatesChicago College of Optometry, Midwestern University, Downers Grove, IL, United StatesChicago College of Pharmacy, Midwestern University, Downers Grove, IL, United StatesSwitch/Sucrose non-fermenting (SWI/SNF) chromatin remodelers hydrolyze ATP to push and slide nucleosomes along the DNA thus modulating access to various genomic loci. These complexes are the most frequently mutated epigenetic regulators in human cancers. SWI/SNF complexes are well known for their function in transcription regulation, but more recent work has uncovered a role for these complexes in the repair of DNA double strand breaks (DSBs). As radiotherapy and most chemotherapeutic agents kill cancer cells by inducing double strand breaks, by identifying a role for these complexes in double strand break repair we are also identifying a DNA repair vulnerability that can be exploited therapeutically in the treatment of SWI/SNF-mutated cancers. In this review we summarize work describing the function of various SWI/SNF subunits in the repair of double strand breaks with a focus on homologous recombination repair and discuss the implication for the treatment of cancers with SWI/SNF mutations.https://www.frontiersin.org/articles/10.3389/fcell.2022.1071786/fullchromatin remodelershomologous recombinationdouble strand break repaircancer therapyDNA end resectionSWI/SNF |
| spellingShingle | Maria Sadek Anand Sheth Grant Zimmerman Emily Hays Renier Vélez-Cruz Renier Vélez-Cruz Renier Vélez-Cruz Renier Vélez-Cruz The role of SWI/SNF chromatin remodelers in the repair of DNA double strand breaks and cancer therapy Frontiers in Cell and Developmental Biology chromatin remodelers homologous recombination double strand break repair cancer therapy DNA end resection SWI/SNF |
| title | The role of SWI/SNF chromatin remodelers in the repair of DNA double strand breaks and cancer therapy |
| title_full | The role of SWI/SNF chromatin remodelers in the repair of DNA double strand breaks and cancer therapy |
| title_fullStr | The role of SWI/SNF chromatin remodelers in the repair of DNA double strand breaks and cancer therapy |
| title_full_unstemmed | The role of SWI/SNF chromatin remodelers in the repair of DNA double strand breaks and cancer therapy |
| title_short | The role of SWI/SNF chromatin remodelers in the repair of DNA double strand breaks and cancer therapy |
| title_sort | role of swi snf chromatin remodelers in the repair of dna double strand breaks and cancer therapy |
| topic | chromatin remodelers homologous recombination double strand break repair cancer therapy DNA end resection SWI/SNF |
| url | https://www.frontiersin.org/articles/10.3389/fcell.2022.1071786/full |
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