The nuclear events of a eukaryotic cell, such as replication, transcription, recombination and repair etc. require the transition of the compactly arranged chromatin into an uncompacted state and vice-versa. This is mediated by post-translational modification of the histones, exchange of histone variants and ATP-dependent chromatin remodeling. The SWI/SNF chromatin remodeling complexes are one of the most well characterized families of chromatin remodelers. In addition to their role in modulating chromatin, they have also been assigned roles in cancer and health-related anomalies such as developmental, neurocognitive, and intellectual disabilities. Owing to their vital cellular and medical connotations, developing an understanding of the structural and functional aspects of the complex becomes imperative. However, due to the intricate nature of higher-order chromatin as well as compositional heterogeneity of the SWI/SNF complex, intra-species isoforms and inter-species homologs, this often becomes challenging. To this end, the present review attempts to present an amalgamated perspective on the discovery, structure, function, and regulation of the SWI/SNF complex.
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http://dx.doi.org/10.1007/s12013-023-01140-5 | DOI Listing |
Sci Rep
January 2025
Department of Physics and Astronomy, Clemson University, Clemson, SC, USA.
The ARID1A gene, frequently mutated in cancer, encodes the AT-rich interactive domain-containing protein 1 A, a key component of the chromatin remodeling SWI/SNF complex. The ARID1A protein features a conserved DNA-binding domain (ARID domain) of approximately 100 residues crucial for its function. Despite the frequency of mutations, the impact on ARID1A's stability and contribution to cancer progression remains unclear.
View Article and Find Full Text PDFJ Pathol
January 2025
SIREDO Oncology Center (Care, Innovation and Research for Children and AYA with Cancer), Institut Curie, Université Paris Cité, Paris, France.
Rhabdoid tumours (RT) are an aggressive malignancy affecting <2-year-old infants, characterised by biallelic loss-of-function alterations in SWI/SNF-related BAF chromatin remodelling complex subunit B1 (SMARCB1) in nearly all cases. Germline SMARCB1 alterations are found in ~30% of patients and define the RT Predisposition Syndrome type 1 (RTPS1). Uveal melanoma (UVM), the most common primary intraocular cancer in adults, does not harbour SMARCB1 alterations.
View Article and Find Full Text PDFCarcinogenesis
January 2025
Department of Pathology, Nanjing Jinling Hospital, Nanjing University School of Medicine, Nanjing, 210002, China.
The tumor suppressor gene SMARCA4, a critical component of the SWI/SNF chromatin remodeling complex, is frequently inactivated in various cancers, including clear cell renal cell carcinoma (ccRCC). Despite its significance, the role of SMARCA4 in ccRCC development and its potential therapeutic vulnerabilities have not been fully explored. Our research found that SMARCA4 deficiency was associated with poor prognosis and was observed in a subset of high-grade ccRCCs.
View Article and Find Full Text PDFRev Physiol Biochem Pharmacol
January 2025
Institute of Medical Sciences, University of Aberdeen, Aberdeen, Scotland, UK.
Multiple epigenetic modulations occur to chromatin rather than to DNA itself and these influence gene expression or gene silencing profoundly. Both the creation of these post-translational modifications and the mechanisms of their readout are regulated significantly by electrical forces several of which are discussed. They are also influenced by phase separation which itself is driven by electrical forces.
View Article and Find Full Text PDFCancer Lett
January 2025
Department of Biochemistry and Molecular Biology; Key Laboratory of Breast Cancer Prevention and Treatment of the Ministry of Education, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center of Cancer, Tianjin 300060, China. Electronic address:
Patients with estrogen receptor-positive (ER+) breast cancer require long-term endocrine therapy. However, endocrine resistance remains a critical issue to be addressed. Herein, we show that ERα repressed FOXF2 transcription in ER+ breast cancer through H3K27me3 modification, therefore endocrine therapy triggered FOXF2 transcription via loss of H3K27me3.
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