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The SWI/SNF chromatin remodelling complex: Its role in maintaining genome stability and preventing tumourigenesis
Peter M Brownlee1, Cornelia Meisenberg1, Jessica A Downs1
1Genome Damage and Stability Centre, University of Sussex, Falmer, Brighton BN1 9RQ, UK.
Abstract:
Genes encoding subunits of the two SWI/SNF chromatin remodelling complexes (BAF and PBAF) are mutated in almost 20% of all human cancers. In addition to a role in regulating transcription, recent work from our laboratory and others identified roles for both complexes in DNA damage responses and the maintenance of sister chromatid cohesion, which may have profound impacts on genome stability and contribute to its role as a tumour suppressor. Here, we review some of the transcription-independent functions of the SWI/SNF chromatin remodelling complex and discuss these in light of their potential relevance to tumourigenesis.
Insights
Mutations in SWI/SNF chromatin remodeling complexes are common in human cancers. These complexes have transcription-independent roles in DNA repair and genome stability, crucial for tumor suppression.
Area of Science:
- Molecular Biology
- Genetics
- Cancer Research
Background:
- SWI/SNF chromatin remodeling complexes (BAF and PBAF) are frequently mutated in human cancers.
- These complexes are known regulators of gene transcription.
- Emerging evidence suggests roles beyond transcription.
Purpose of the Study:
- To review transcription-independent functions of SWI/SNF complexes.
- To discuss the relevance of these functions to cancer development.
Main Methods:
- Literature review of recent studies on SWI/SNF complexes.
- Analysis of experimental data linking SWI/SNF to DNA damage response and sister chromatid cohesion.
Main Results:
- SWI/SNF complexes play critical roles in DNA damage responses.
- These complexes are essential for maintaining sister chromatid cohesion.
- These functions impact genome stability.
Conclusions:
- Transcription-independent functions of SWI/SNF complexes are vital for genome stability.
- Dysregulation of these functions may contribute to tumorigenesis.
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