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Artykuły w czasopismach na temat „Complexe SWItch/Sucrose Non-Fermentable”

Autor: Grafiati

Data publikacji: 16 listopada 2024

Data aktualizacji: 31 lipca 2025

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1

Choi, Sung Kyung, Myoung Jun Kim, and Jueng Soo You. "SMARCB1 Acts as a Quiescent Gatekeeper for Cell Cycle and Immune Response in Human Cells." International Journal of Molecular Sciences 21, no. 11 (2020): 3969. http://dx.doi.org/10.3390/ijms21113969.

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Switch/sucrose non-fermentable (SWI/SNF)-related matrix-associated actin-dependent regulator of chromatin (SMARC) subfamily B member 1 (SMARCB1) is a core subunit of the switch/sucrose non-fermentable (SWI/SNF) complex, one of the adenosine triphosphate (ATP)-dependent chromatin remodeler complexes. The unique role of SMARCB1 has been reported in various cellular contexts. Here, we focused on the general role of the ubiquitous expression of SMARCB1 in a normal cell state. We selected ARPE19 (human primary retinal pigment epithelium) and IMR90 (from human fetal lung fibroblasts) cell lines as t

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Nguyen, Thinh T., Joanne G. A. Savory, Travis Brooke-Bisschop, et al. "Cdx2 Regulates Gene Expression through Recruitment of Brg1-associated Switch-Sucrose Non-fermentable (SWI-SNF) Chromatin Remodeling Activity." Journal of Biological Chemistry 292, no. 8 (2017): 3389–99. http://dx.doi.org/10.1074/jbc.m116.752774.

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The packaging of genomic DNA into nucleosomes creates a barrier to transcription that can be relieved through ATP-dependent chromatin remodeling via complexes such as the switch-sucrose non-fermentable (SWI-SNF) chromatin remodeling complex. The SWI-SNF complex remodels chromatin via conformational or positional changes of nucleosomes, thereby altering the access of transcriptional machinery to target genes. The SWI-SNF complex has limited ability to bind to sequence-specific elements, and, therefore, its recruitment to target loci is believed to require interaction with DNA-associated transcr

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Liu, Hongyu, Yang Zhao, Guizhen Zhao, Yongjie Deng, Y. Eugene Chen, and Jifeng Zhang. "SWI/SNF Complex in Vascular Smooth Muscle Cells and Its Implications in Cardiovascular Pathologies." Cells 13, no. 2 (2024): 168. http://dx.doi.org/10.3390/cells13020168.

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Mature vascular smooth muscle cells (VSMC) exhibit a remarkable degree of plasticity, a characteristic that has intrigued cardiovascular researchers for decades. Recently, it has become increasingly evident that the chromatin remodeler SWItch/Sucrose Non-Fermentable (SWI/SNF) complex plays a pivotal role in orchestrating chromatin conformation, which is critical for gene regulation. In this review, we provide a summary of research related to the involvement of the SWI/SNF complexes in VSMC and cardiovascular diseases (CVD), integrating these discoveries into the current landscape of epigenetic

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Rembiałkowska, Nina, Katarzyna Rekiel, Piotr Urbanowicz, et al. "Epigenetic Dysregulation in Cancer: Implications for Gene Expression and DNA Repair-Associated Pathways." International Journal of Molecular Sciences 26, no. 13 (2025): 6531. https://doi.org/10.3390/ijms26136531.

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Epigenetic modifications are heritable, reversible alterations that causally reshape chromatin architecture and thereby influence DNA repair without changing nucleotide sequence. DNA methylation, histone modifications and non-coding RNAs profoundly influence DNA repair mechanisms and genomic stability. Aberrant epigenetic patterns in cancer compromise DNA damage recognition and repair, therefore impairing homologous recombination (HR), non-homologous end joining (NHEJ), and base excision repair (BER) by suppressing key repair genes and lowering access to repair sites. Then it is dissected how

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Del Savio, Elisa, and Roberta Maestro. "Beyond SMARCB1 Loss: Recent Insights into the Pathobiology of Epithelioid Sarcoma." Cells 11, no. 17 (2022): 2626. http://dx.doi.org/10.3390/cells11172626.

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Epithelioid sarcoma (ES) is a very rare and aggressive mesenchymal tumor of unclear origin and uncertain lineage characterized by a prevalent epithelioid morphology. The only recurrent genetic alteration reported in ES as yet is the functional inactivation of SMARCB1 (SWI/SNF-related matrix-associated actin-dependent regulator of chromatin subfamily B member 1), a key component of the SWI/SNF (SWItch/Sucrose Non-Fermentable) chromatin remodeling complexes. How SMARCB1 deficiency dictates the clinicopathological characteristics of ES and what other molecular defects concur to its malignant prog

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Wanior, Marek, Andreas Krämer, Stefan Knapp, and Andreas C. Joerger. "Exploiting vulnerabilities of SWI/SNF chromatin remodelling complexes for cancer therapy." Oncogene 40, no. 21 (2021): 3637–54. http://dx.doi.org/10.1038/s41388-021-01781-x.

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AbstractMulti-subunit ATPase-dependent chromatin remodelling complexes SWI/SNF (switch/sucrose non-fermentable) are fundamental epigenetic regulators of gene transcription. Functional genomic studies revealed a remarkable mutation prevalence of SWI/SNF-encoding genes in 20–25% of all human cancers, frequently driving oncogenic programmes. Some SWI/SNF-mutant cancers are hypersensitive to perturbations in other SWI/SNF subunits, regulatory proteins and distinct biological pathways, often resulting in sustained anticancer effects and synthetic lethal interactions. Exploiting these vulnerabilitie

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Soto-Castillo, Juan José, Lucía Llavata-Marti, Roser Fort-Culillas, et al. "SWI/SNF Complex Alterations in Tumors with Rhabdoid Features: Novel Therapeutic Approaches and Opportunities for Adoptive Cell Therapy." International Journal of Molecular Sciences 24, no. 13 (2023): 11143. http://dx.doi.org/10.3390/ijms241311143.

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The SWItch/Sucrose Non-Fermentable (SWI/SNF) chromatin-remodeling complex is one of the most remarkably altered epigenetic regulators in cancer. Pathogenic mutations in genes encoding SWI/SNF-related proteins have been recently described in many solid tumors, including rare and aggressive malignancies with rhabdoid features with no standard therapies in advanced or metastatic settings. In recent years, clinical trials with targeted drugs aimed at restoring its function have shown discouraging results. However, preclinical data have found an association between these epigenetic alterations and

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Hasan, Nesrin, and Nita Ahuja. "The Emerging Roles of ATP-Dependent Chromatin Remodeling Complexes in Pancreatic Cancer." Cancers 11, no. 12 (2019): 1859. http://dx.doi.org/10.3390/cancers11121859.

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Pancreatic cancer is an aggressive cancer with low survival rates. Genetic and epigenetic dysregulation has been associated with the initiation and progression of pancreatic tumors. Multiple studies have pointed to the involvement of aberrant chromatin modifications in driving tumor behavior. ATP-dependent chromatin remodeling complexes regulate chromatin structure and have critical roles in stem cell maintenance, development, and cancer. Frequent mutations and chromosomal aberrations in the genes associated with subunits of the ATP-dependent chromatin remodeling complexes have been detected i

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9

Collingwood, TN, FD Urnov, and AP Wolffe. "Nuclear receptors: coactivators, corepressors and chromatin remodeling in the control of transcription." Journal of Molecular Endocrinology 23, no. 3 (1999): 255–75. http://dx.doi.org/10.1677/jme.0.0230255.

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A contemporary view of hormone action at the transcriptional level requires knowledge of the transcription factors including the hormone receptor that may bind to promoters or enhancers, together with the chromosomal context within which these regulatory proteins function. Nuclear receptors provide the best examples of transcriptional control through the targeted recruitment of large protein complexes that modify chromosomal components and reversibly stabilize or destabilize chromatin. Ligand-dependent recruitment of transcriptional coactivators destabilizes chromatin by mechanisms including h

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10

Padilla-Benavides, Teresita, Pablo Reyes-Gutierrez, and Anthony N. Imbalzano. "Regulation of the Mammalian SWI/SNF Family of Chromatin Remodeling Enzymes by Phosphorylation during Myogenesis." Biology 9, no. 7 (2020): 152. http://dx.doi.org/10.3390/biology9070152.

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Myogenesis is the biological process by which skeletal muscle tissue forms. Regulation of myogenesis involves a variety of conventional, epigenetic, and epigenomic mechanisms that control chromatin remodeling, DNA methylation, histone modification, and activation of transcription factors. Chromatin remodeling enzymes utilize ATP hydrolysis to alter nucleosome structure and/or positioning. The mammalian SWItch/Sucrose Non-Fermentable (mSWI/SNF) family of chromatin remodeling enzymes is essential for myogenesis. Here we review diverse and novel mechanisms of regulation of mSWI/SNF enzymes by kin

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11

Wu, Shuai, Nail Fatkhutdinov, Leah Rosin, et al. "ARID1A spatially partitions interphase chromosomes." Science Advances 5, no. 5 (2019): eaaw5294. http://dx.doi.org/10.1126/sciadv.aaw5294.

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ARID1A, a subunit of the SWItch/Sucrose Non-Fermentable (SWI/SNF) chromatin-remodeling complex, localizes to both promoters and enhancers to influence transcription. However, the role of ARID1A in higher-order spatial chromosome partitioning and genome organization is unknown. Here, we show that ARID1A spatially partitions interphase chromosomes and regulates higher-order genome organization. The SWI/SNF complex interacts with condensin II, and they display significant colocalizations at enhancers. ARID1A knockout drives the redistribution of condensin II preferentially at enhancers, which pos

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Cruz-Tapia, Roberto Onner, Ana María Cano-Valdez, Abelardo Meneses-García, et al. "Switch/Sucrose Non-Fermentable (SWI/SNF) Complex—Partial Loss in Sinonasal Squamous Cell Carcinoma: A High-Grade Morphology Impact and Progression." Current Issues in Molecular Biology 46, no. 11 (2024): 12183–95. http://dx.doi.org/10.3390/cimb46110723.

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Sinonasal carcinomas are aggressive neoplasms that present a high morbidity and mortality rate with an unfavorable prognosis. This group of tumors exhibits morphological and genetic diversity. Genetic and epigenetic alterations in these neoplasms are the current targets for diagnosis and treatment. The most common type of cancer originating in the sinonasal tract is sinonasal squamous cell carcinomas (SNSCCs), which present different histological patterns and variable histological aggressiveness. A significant number of alterations have been reported in sinonasal tumors, including deficiencies

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13

Ngo, Carine, and Sophie Postel-Vinay. "Immunotherapy for SMARCB1-Deficient Sarcomas: Current Evidence and Future Developments." Biomedicines 10, no. 3 (2022): 650. http://dx.doi.org/10.3390/biomedicines10030650.

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Mutations in subunits of the SWItch Sucrose Non-Fermentable (SWI/SNF) complex occur in 20% of all human tumors. Among these, the core subunit SMARCB1 is the most frequently mutated, and SMARCB1 loss represents a founder driver event in several malignancies, such as malignant rhabdoid tumors (MRT), epithelioid sarcoma, poorly differentiated chordoma, and renal medullary carcinoma (RMC). Intriguingly, SMARCB1-deficient pediatric MRT and RMC have recently been reported to be immunogenic, despite their very simple genome and low tumor mutational burden. Responses to immune checkpoint inhibitors ha

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14

Luo, Qingyu, Xiaowei Wu, Wan Chang, et al. "ARID1A Hypermethylation Disrupts Transcriptional Homeostasis to Promote Squamous Cell Carcinoma Progression." Cancer Research 80, no. 3 (2020): 406–17. http://dx.doi.org/10.1158/0008-5472.can-18-2446.

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Abstract Switch/Sucrose Non-Fermentable (SWI/SNF) chromatin-remodeling complexes have a mutation rate of approximately 20% in human cancer, and ARID1A is the most frequently mutated component. However, some components of SWI/SNF complexes, including ARID1A, exhibit a very low mutation rate in squamous cell carcinoma (SCC), and their role in SCC remains unknown. Here, we demonstrate that the low expression of ARID1A in SCC is the result of promoter hypermethylation. Low levels of ARID1A were associated with a poor prognosis. ARID1A maintained transcriptional homeostasis through both direct and

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15

Li, Jing Jing, and Cheok Soon Lee. "The Role of the AT-Rich Interaction Domain 1A Gene (ARID1A) in Human Carcinogenesis." Genes 15, no. 1 (2023): 5. http://dx.doi.org/10.3390/genes15010005.

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The switch/sucrose non-fermentable (SWI/SNF) (SWI/SNF) complex uses energy from ATP hydrolysis to mobilise nucleosomes on chromatin. Components of SWI/SNF are mutated in 20% of all human cancers, of which mutations in AT-rich binding domain protein 1A (ARID1A) are the most common. ARID1A is mutated in nearly half of ovarian clear cell carcinoma and around one-third of endometrial and ovarian carcinomas of the endometrioid type. This review will examine in detail the molecular functions of ARID1A, including its role in cell cycle control, enhancer regulation, and the prevention of telomerase ac

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El Hadidy and Uversky. "Intrinsic Disorder of the BAF Complex: Roles in Chromatin Remodeling and Disease Development." International Journal of Molecular Sciences 20, no. 21 (2019): 5260. http://dx.doi.org/10.3390/ijms20215260.

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The two-meter-long DNA is compressed into chromatin in the nucleus of every cell, which serves as a significant barrier to transcription. Therefore, for processes such as replication and transcription to occur, the highly compacted chromatin must be relaxed, and the processes required for chromatin reorganization for the aim of replication or transcription are controlled by ATP-dependent nucleosome remodelers. One of the most highly studied remodelers of this kind is the BRG1- or BRM-associated factor complex (BAF complex, also known as SWItch/sucrose non-fermentable (SWI/SNF) complex), which

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Hu, Xiaolong, Mengjie Li, Xue Hao, Yi Lu, Lei Zhang, and Geng Wu. "The Osa-Containing SWI/SNF Chromatin-Remodeling Complex Is Required in the Germline Differentiation Niche for Germline Stem Cell Progeny Differentiation." Genes 12, no. 3 (2021): 363. http://dx.doi.org/10.3390/genes12030363.

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The Drosophila ovary is recognized as a powerful model to study stem cell self-renewal and differentiation. Decapentaplegic (Dpp) is secreted from the germline stem cell (GSC) niche to activate Bone Morphogenic Protein (BMP) signaling in GSCs for their self-renewal and is restricted in the differentiation niche for daughter cell differentiation. Here, we report that Switch/sucrose non-fermentable (SWI/SNF) component Osa depletion in escort cells (ECs) results in a blockage of GSC progeny differentiation. Further molecular and genetic analyses suggest that the defective germline differentiation

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Crodian, Jennifer S., Bethany M. Weldon, Yu-Chun Tseng, Birgit Cabot, and Ryan Cabot. "Nuclear trafficking dynamics of Bromodomain-containing protein 7 (BRD7), a switch/sucrose non-fermentable (SWI/SNF) chromatin remodelling complex subunit, in porcine oocytes and cleavage-stage embryos." Reproduction, Fertility and Development 31, no. 9 (2019): 1497. http://dx.doi.org/10.1071/rd19030.

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In the work presented here, we investigated how bromodomain-containing protein 7 (BRD7), a subunit associated with switch/sucrose non-fermentable (SWI/SNF) chromatin remodelling complexes, is trafficked between cellular compartments during embryo development. SWI/SNF complexes are multi-subunit complexes that contain a core catalytic subunit (SWI/SNF related, Matrix associated, Actin dependent Regulator of Chromatin, subfamily A, member 4, or member 2; SMARCA4 or SMARCA2) and a collection of additional subunits that guide the complexes to their appropriate loci; BRD7 is one of these additional

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Kang, Jong-Seol, Dongha Kim, Joonwoo Rhee, et al. "Baf155 regulates skeletal muscle metabolism via HIF-1a signaling." PLOS Biology 21, no. 7 (2023): e3002192. http://dx.doi.org/10.1371/journal.pbio.3002192.

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During exercise, skeletal muscle is exposed to a low oxygen condition, hypoxia. Under hypoxia, the transcription factor hypoxia-inducible factor-1α (HIF-1α) is stabilized and induces expressions of its target genes regulating glycolytic metabolism. Here, using a skeletal muscle-specific gene ablation mouse model, we show that Brg1/Brm-associated factor 155 (Baf155), a core subunit of the switch/sucrose non-fermentable (SWI/SNF) complex, is essential for HIF-1α signaling in skeletal muscle. Muscle-specific ablation of Baf155 increases oxidative metabolism by reducing HIF-1α function, which acco

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Peinado, Paola, Alvaro Andrades, Marta Cuadros, et al. "Comprehensive Analysis of SWI/SNF Inactivation in Lung Adenocarcinoma Cell Models." Cancers 12, no. 12 (2020): 3712. http://dx.doi.org/10.3390/cancers12123712.

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Mammalian SWI/SNF (SWitch/Sucrose Non-Fermentable) complexes are ATP-dependent chromatin remodelers whose subunits have emerged among the most frequently mutated genes in cancer. Studying SWI/SNF function in cancer cell line models has unveiled vulnerabilities in SWI/SNF-mutant tumors that can lead to the discovery of new therapeutic drugs. However, choosing an appropriate cancer cell line model for SWI/SNF functional studies can be challenging because SWI/SNF subunits are frequently altered in cancer by various mechanisms, including genetic alterations and post-transcriptional mechanisms. In

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Ma, Yue, Natisha R. Field, Tao Xie, et al. "Aberrant SWI/SNF Complex Members Are Predominant in Rare Ovarian Malignancies—Therapeutic Vulnerabilities in Treatment-Resistant Subtypes." Cancers 16, no. 17 (2024): 3068. http://dx.doi.org/10.3390/cancers16173068.

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SWI/SNF (SWItch/Sucrose Non-Fermentable) is the most frequently mutated chromatin-remodelling complex in human malignancy, with over 20% of tumours having a mutation in a SWI/SNF complex member. Mutations in specific SWI/SNF complex members are characteristic of rare chemoresistant ovarian cancer histopathological subtypes. Somatic mutations in ARID1A, encoding one of the mutually exclusive DNA-binding subunits of SWI/SNF, occur in 42–67% of ovarian clear cell carcinomas (OCCC). The concomitant somatic or germline mutation and epigenetic silencing of the mutually exclusive ATPase subunits SMAR

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Angelico, Giuseppe, Giulio Attanasio, Lorenzo Colarossi, et al. "ARID1A Mutations in Gastric Cancer: A Review with Focus on Clinicopathological Features, Molecular Background and Diagnostic Interpretation." Cancers 16, no. 11 (2024): 2062. http://dx.doi.org/10.3390/cancers16112062.

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AT-rich interaction domain 1 (ARID1A) is a pivotal gene with a significant role in gastrointestinal tumors which encodes a protein referred to as BAF250a or SMARCF1, an integral component of the SWI/SNF (SWItch/sucrose non-fermentable) chromatin remodeling complex. This complex is instrumental in regulating gene expression by modifying the structure of chromatin to affect the accessibility of DNA. Mutations in ARID1A have been identified in various gastrointestinal cancers, including colorectal, gastric, and pancreatic cancers. These mutations have the potential to disrupt normal SWI/SNF compl

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Xiao, Lanbo, Abhijit Parolia, Yuanyuan Qiao, et al. "Targeting SWI/SNF ATPases in enhancer-addicted prostate cancer." Nature 601, no. 7893 (2021): 434–39. http://dx.doi.org/10.1038/s41586-021-04246-z.

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AbstractThe switch/sucrose non-fermentable (SWI/SNF) complex has a crucial role in chromatin remodelling1 and is altered in over 20% of cancers2,3. Here we developed a proteolysis-targeting chimera (PROTAC) degrader of the SWI/SNF ATPase subunits, SMARCA2 and SMARCA4, called AU-15330. Androgen receptor (AR)+ forkhead box A1 (FOXA1)+ prostate cancer cells are exquisitely sensitive to dual SMARCA2 and SMARCA4 degradation relative to normal and other cancer cell lines. SWI/SNF ATPase degradation rapidly compacts cis-regulatory elements bound by transcription factors that drive prostate cancer cel

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Ito, Taiji, Hirotaka Watanabe, Nobutake Yamamichi, et al. "Brm transactivates the telomerase reverse transcriptase (TERT) gene and modulates the splicing patterns of its transcripts in concert with p54nrb." Biochemical Journal 411, no. 1 (2008): 201–9. http://dx.doi.org/10.1042/bj20071075.

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We report that a DBHS (Drosophila behaviour, human splicing) family protein, p54nrb, binds both BRG1 (Brahma-related gene 1) and Brm (Brahma), catalytic subunits of the SWI/SNF (switch/sucrose non-fermentable) chromatin remodelling complex, and also another core subunit of this complex, BAF60a. The N-terminal region of p54nrb is sufficient to pull-down other core subunits of the SWI/SNF complex, suggesting that p54nrb binds SWI/SNF-like complexes. PSF (polypyrimidine tract-binding protein-associated splicing factor), another DBHS family protein known to directly bind p54nrb, was also found to

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Krishnamurthy, Nithya, Shumei Kato, Scott Lippman, and Razelle Kurzrock. "Chromatin remodeling (SWI/SNF) complexes, cancer, and response to immunotherapy." Journal for ImmunoTherapy of Cancer 10, no. 9 (2022): e004669. http://dx.doi.org/10.1136/jitc-2022-004669.

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Chromatin regulation involves four subfamilies composed of ATP-dependent multifunctional protein complexes that remodel the way DNA is packaged. The SWItch/Sucrose Non-Fermentable (SWI/SNF) chromatin remodeling complex subfamily mediates nucleosome reorganization and hence activation/repression of critical genes. The SWI/SNF complex is composed of the BRG-/BRM-associated factor and Polybromo-associated BAF complexes, which in turn have multiple subunits. Significantly, ~20% of malignancies harbor alterations in >1 of these subunits, making the genes encoding SWI/SNF family members among the

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Chinnaiyan, Arul M. "Abstract IA021: Targeting epigenetic regulators of oncogenic transcription factors." Cancer Research 82, no. 23_Supplement_2 (2022): IA021. http://dx.doi.org/10.1158/1538-7445.cancepi22-ia021.

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Abstract The switch/sucrose non-fermentable (SWI/SNF) complex has a crucial role in chromatin remodeling and is altered in over 20% of cancers. We recently developed and evaluated a proteolysis-targeting chimera (PROTAC) degrader of the SWI/SNF ATPase subunits, SMARCA2 and SMARCA4, called AU-15330. Androgen receptor (AR)+ forkhead box A1 (FOXA1)+ prostate cancer cells are exquisitely sensitive to dual SMARCA2 and SMARCA4 degradation relative to normal and other cancer cell lines. SWI/SNF ATPase degradation rapidly compacts cis-regulatory elements bound by transcription factors that drive prost

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Xu, Mingyan, Junling Zhang, Xuemei Lu, Fan Liu, Songlin Shi, and Xiaoling Deng. "MiR-199a-5p-Regulated SMARCA4 Promotes Oral Squamous Cell Carcinoma Tumorigenesis." International Journal of Molecular Sciences 24, no. 5 (2023): 4756. http://dx.doi.org/10.3390/ijms24054756.

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SWI/SNF related, matrix associated, actin-dependent regulator of chromatin, subfamily a, member 4 (SMARCA4, also known as BRG1), an ATPase subunit of the switch/sucrose non-fermentable (SWI/SNF) chromatin remodeling complex, plays an important regulatory role in many cytogenetic and cytological processes during cancer development. However, the biological function and mechanism of SMARCA4 in oral squamous cell carcinoma (OSCC) remain unclear. The present study aimed to investigate the role of SMARCA4 in OSCC and its potential mechanism. Using a tissue microarray, SMARCA4 expression was found to

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Wang, Wenjia, Scott C. Friedland, Bing Guo, et al. "ARID1A, a SWI/SNF subunit, is critical to acinar cell homeostasis and regeneration and is a barrier to transformation and epithelial-mesenchymal transition in the pancreas." Gut 68, no. 7 (2018): 1245–58. http://dx.doi.org/10.1136/gutjnl-2017-315541.

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ObjectiveHere, we evaluate the contribution of AT-rich interaction domain-containing protein 1A (ARID1A), the most frequently mutated member of the SWItch/sucrose non-fermentable (SWI/SNF) complex, in pancreatic homeostasis and pancreatic ductal adenocarcinoma (PDAC) pathogenesis using mouse models.DesignMice with a targeted deletion of Arid1a in the pancreas by itself and in the context of two common genetic alterations in PDAC, Kras and p53, were followed longitudinally. Pancreases were examined and analysed for proliferation, response to injury and tumourigenesis. Cancer cell lines derived

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Guo, Ao, Hongling Huang, Zhexin Zhu, et al. "The SWI/SNF canonical BAF complex and c-Myc cooperate to promote early fate decisions in CD8+ T cells." Journal of Immunology 208, no. 1_Supplement (2022): 169.02. http://dx.doi.org/10.4049/jimmunol.208.supp.169.02.

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Abstract The identification of mechanisms to promote the generation of memory T cells (TMEM) has important implications for vaccination and anti-cancer immunotherapy. Using a CRISPR-based screen for negative regulators of TMEM generation in vivo, we discovered many components of the mammalian canonical SWItch/Sucrose Non-Fermentable (SWI/SNF) complex, also called canonical Brg1/Brg-associated factor (cBAF). cBAF is essential for the differentiation of activated, naïve CD8+ T cells into T effector (TEFF) cells, and loss of cBAF promotes TMEM formation of CD8+ T cells in vivo upon infection with

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Van Rechem, Capucine. "EPCO-43. CHROMATIN REMODELERS LOST IN TRANSLATION." Neuro-Oncology 24, Supplement_7 (2022): vii125—vii126. http://dx.doi.org/10.1093/neuonc/noac209.477.

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Abstract The chromatin remodeler complexes mammalian SWI/SNF (SWItch/Sucrose Non-Fermentable) are altered in more than 40% of cancers and are involved in therapeutic resistance. In children,SMARCB1 is mutated in 95% of rhabdoid tumors, and the remaining 5% present mutations in SMARCA4. These tumors are typically identified in children younger than three years old and have a very poor prognosis with a survival under one year following diagnosis. SMARCB1 expression is also lost in more than 90% of epithelial sarcomas, a rare and aggressive tumor affecting young adults, and in 50% of pediatric ch

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Van Rechem, Capucine. "BIOL-04. FROM MSWI/SNF’S ROLES IN PROTEIN SYNTHESIS TO NEW THERAPEUTIC OPPORTUNITIES." Neuro-Oncology 25, Supplement_1 (2023): i6. http://dx.doi.org/10.1093/neuonc/noad073.023.

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Abstract The chromatin remodeler complexes mammalian SWI/SNF (SWItch/Sucrose Non-Fermentable) are altered in more than 40% of cancers and are involved in therapeutic resistance. In children, SMARCB1 is mutated in 95% of rhabdoid tumors, and the remaining 5% present mutations in SMARCA4. These tumors are typically identified in children younger than three years old and have a very poor prognosis with a survival under one year following diagnosis. SMARCB1 expression is also lost in more than 90% of epithelial sarcomas, a rare and aggressive tumor affecting young adults, and in 50% of pediatric c

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Yao, Xiaosai, Jing Han Hong, Amrita Nargund та Bin Tean Teh. "Abstract B006: PBRM1-deficient PBAF complexes target de novo genomic loci to activate NF-κB pathway in kidney cancer". Cancer Research 82, № 23_Supplement_2 (2022): B006. http://dx.doi.org/10.1158/1538-7445.cancepi22-b006.

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Abstract Polybromo-1 (PBRM1) is the second most commonly mutated gene in kidney cancer after VHL, occurring at a frequency of 30-40%. PBRM1 loss represents a tumor-initiating event and the combined loss of VHL and PBRM1 is necessary and sufficient for renal malignancy. Functionally, PBRM1 is the defining subunit of the polybromo BRG1-associated factor (PBAF) subclass of SWItch/Sucrose Non-Fermentable (SWI/SNF) remodeling complex which regulates chromatin accessibility by sliding, depositing or evicting nucleosomes. Determining context-specific chromatin remodeling by PBRM1 is paramount to unde

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Pawel, Bruce R. "SMARCB1-deficient Tumors of Childhood: A Practical Guide." Pediatric and Developmental Pathology 21, no. 1 (2017): 6–28. http://dx.doi.org/10.1177/1093526617749671.

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The SMARCB1 gene ( INI1, BAF47) is a member of the SWItch/Sucrose Non-Fermentable (SWI/SNF) chromatin remodeling complex, involved in the epigenetic regulation of gene transcription. SMARCB1 acts as a tumor suppressor gene, and loss of function of both alleles gives rise to SMARCB1-deficient tumors. The prototypical SMARCB1-deficient tumor is the malignant rhabdoid tumor (MRT) which was first described in the kidney but also occurs in soft tissue, viscera, and the brain (where it is referred to as atypical teratoid rhabdoid tumor or AT/RT). These are overwhelmingly tumors of the very young, an

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Gong, Wangqiu, Congwei Luo, Fenfen Peng та ін. "Brahma-related gene-1 promotes tubular senescence and renal fibrosis through Wnt/β-catenin/autophagy axis". Clinical Science 135, № 15 (2021): 1873–95. http://dx.doi.org/10.1042/cs20210447.

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Abstract Although accelerated cellular senescence is closely related to the progression of chronic kidney disease (CKD) and renal fibrosis, the underlying mechanisms remain largely unknown. Here, we reported that tubular aberrant expression of Brahma-related gene 1 (BRG1), an enzymatic subunit of the SWItch/Sucrose Non-Fermentable complex, is critically involved in tubular senescence and renal fibrosis. BRG1 was significantly up-regulated in the kidneys, predominantly in tubular epithelial cells, of both CKD patients and unilateral ureteral obstruction (UUO) mice. In vivo, shRNA-mediated knock

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Halaoui, Adham, Najla Kfoury-Beaumont, and Thomas Beaumont. "Abstract B011: Sex-specific chromatin remodeling drives tumorigenesis in glioblastoma." Cancer Research 84, no. 5_Supplement_1 (2024): B011. http://dx.doi.org/10.1158/1538-7445.brain23-b011.

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Abstract SWItch/Sucrose Non-Fermentable (SWI/SNF) chromatin remodelling complexes are potent regulators of cellular differentiation that are encoded by some of the most frequently altered genes in cancer. Within this family, the ATP-dependent (BRG-1/BRM associated factor (BAF) chromatin remodelling complex is altered in roughly 20% of human cancers including gliomas. However, its role in gliomagenesis and progression remains largely unknown. The complex exists in three forms: canonical BAF (BAF), polybromo-associated BAF (PBAF) and a non-canonical BAF cmplex (ncBAF), with specific subunits spe

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Morin, Andrew, Darya Wodetzki, Bethany Veo, et al. "ATRT-24. CDK7 Inhibition in AT/RT." Neuro-Oncology 24, Supplement_1 (2022): i8. http://dx.doi.org/10.1093/neuonc/noac079.023.

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Abstract Atypical teratoid/rhabdoid tumors (AT/RT) are CNS tumors with a 5-year survival of ~35%. AT/RT is characterized by loss-of-function mutations in the SMARCB1 component of the SWI/SNF (SWItch/Sucrose Non-Fermentable) complex. Based on preliminary CRISPR-Cas9 gene essentiality screen results identifying AT/RT vulnerabilities, we hypothesized that interaction between CDK7 and the SWI/SNF complex via SMARCB1 provides a potential target to improve clinical survival of patients. CDK7 expression was identified by microarray in AT/RT, medulloblastoma, glioblastoma and normal brain. Established

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Abraham, Ajay, Daniela Samaniego-Castruita, Jillian Paladino, et al. "Loss of SWI/SNF Complex Subunit Arid1a in B Cells Promotes Inflammation and Perturbs Germinal Center B Cell Responses." Blood 142, Supplement 1 (2023): 1400. http://dx.doi.org/10.1182/blood-2023-189789.

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The Switch/Sucrose Non-Fermentable (SWI/SNF) complex is a major mediator of nucleosomal remodeling in eukaryotic genomes and plays a crucial role in the regulation of chromatin accessibility and establishment of gene expression programs. SWI/SNF complex is comprised of ~15 protein subunits, many of which are frequently mutated in several solid tumors and hematological malignancies, including B cell lymphomas. Among SWI/SNF subunits, ARID1a, ARID1B, and SMARCA4 are each mutated in ~10% of Diffuse Large B-Cell Lymphomas, which is a germinal center B cell-derived malignancy representing 95% of al

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Mota, Mateus, Stefan Sweha, Matt Pun, et al. "Abstract PR-007: H3.3K27M diffuse midline gliomas are sensitive to SWI/SNF chromatin remodeler degradation." Cancer Research 84, no. 5_Supplement_1 (2024): PR—007—PR—007. http://dx.doi.org/10.1158/1538-7445.brain23-pr-007.

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Abstract Diffuse Midline Gliomas (DMG) including Diffuse Intrinsic Pontine Glioma (DIPG) is a lethal pediatric brain tumor. The lysine 27 (K27)-to-methionine (M) point mutation in histone H3.1 or H3.3 (H3.1K27M or H3.3K27M, respectively) affects about 80% of patients establishing H3K27M mutation as a tumor hallmark. Mutated H3 histones inhibit the function of Polycomb repressive complex 2 resulting in global reduction of repressive H3K27me3. In addition, increased acetylation of H3K27 is observed, further contributing to an aberrant chromatin state. Considering the impact of epigenetic alterat

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Basu, Gargi D., Tracey White, Janine R. LoBello, et al. "ARID1A alterations in gastrointestinal cancers as therapeutic opportunities." Journal of Clinical Oncology 34, no. 4_suppl (2016): 671. http://dx.doi.org/10.1200/jco.2016.34.4_suppl.671.

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671 Background: The gene encoding the AT-rich interacting domain (ARID1A) is a tumor suppressor and a subunit of the Switch/Sucrose Non fermentable (SWI/SNF) chromatin remodeling complex that regulates gene expression. Additionally, ARID1A functions to maintain genomic integrity by interacting with ATR. Mutations in ARID1A have been observed in a number of cancers. Inactivation of ARID1A has been reported to lead to increased sensitivity to inhibitors of PARP and PI3K/AKT pathway. We evaluated ARID1A alterations in gastrointestinal (GI) cancers to identify new therapeutic options. Methods: Com

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Machado, Annette Alexandra, Prit Benny Malgulwar, and Jason T. Huse. "EPCO-21. ELUCIDATING THE FUNCTIONAL RELEVANCE OF ATRX-DEFICIENCY IN H3.3-G34-MUTANT DIFFUSE HEMISPHERIC GLIOMA." Neuro-Oncology 26, Supplement_8 (2024): viii5. http://dx.doi.org/10.1093/neuonc/noae165.0020.

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Abstract Diffuse hemispheric gliomas (DHGs) account for 30% of aggressive cerebral tumors in children and young adults, exhibiting abysmal outcomes. Co-existing recurrent mutations in H3.3 histones at residue G34 (H3.3-G34R/V mutation) and concurrent inactivating mutations in TP53 and α-thalassemia/intellectual disability-X-linked gene (ATRX) implicate a coordinated molecular effort to drive oncogenesis. ATRX, a core component of the SWItch/Sucrose Non-Fermentable chromatin remodeling complex, regulates the incorporation of histone H3.3 into chromatin sites across the genome to maintain epigen

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Elzamly, S., A. Murzabdillaeva, H. Taha, M. Shitawi, and H. Zhu. "SMARCA4 Deficient Thoracic Sarcoma Presenting with a Pathologic Fracture of Proximal Tibia and L5 Vertebral Body: a Case Report and Review of Literature." American Journal of Clinical Pathology 154, Supplement_1 (2020): S40—S41. http://dx.doi.org/10.1093/ajcp/aqaa161.085.

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Abstract Introduction/Objective SMARCA4 (BRG1) is a central component of the Switch/Sucrose-Non-Fermentable (SWI/SNF) chromatin remodeling complex which plays a critical role in the initiation, progression and dedifferentiation of a variety of cancers arising in different anatomical sites. The recently discovered SMARCA4-deficient thoracic sarcoma (DTS) can present as a mediastinal, pleural or pulmonary mass and constitutes a unique and highly lethal entity. Methods Here we present an interesting case of a 66-year-old, smoker male with past medical history of COPD, polysubstance abuse, hepatit

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Hancock, Wayne W., Yan Xiong, Liqing Wang, et al. "Abstract 6041: Targeting the NuRD component, CHD4, impairs Foxp3+ Treg cell production and function and promotes anti-tumor immunity." Cancer Research 85, no. 8_Supplement_1 (2025): 6041. https://doi.org/10.1158/1538-7445.am2025-6041.

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Abstract Chromatin remodeling enzymes, which reposition nucleosomes throughout the genome to regulate transcription and other processes, include 4 families: chromodomain helicase DNA-binding (CHD), switch/sucrose non-fermentable (SWI/SNF), imitation switch (ISWI), and inositol requiring 80 (INO80). CHD4, a ubiquitous and abundant chromatin remodeling enzyme essential for normal development across a range of tissues, and that is overexpressed in various cancers, is a core member of the nucleosome remodeling and deacetylase (NuRD) complex. Though originally described as a transcriptional repress

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Parolia, Abhijit, Lanbo Xiao, Yuanyuan Qiao, et al. "Abstract 3592: Targeting SWI/SNF ATPases in enhancer-addicted human cancers." Cancer Research 82, no. 12_Supplement (2022): 3592. http://dx.doi.org/10.1158/1538-7445.am2022-3592.

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Abstract In mammalian cells, DNA is wrapped around histone octamers (collectively referred to as nucleosomes) which form a physical barrier to all DNA-based processes. The switch/sucrose non-fermentable (SWI/SNF) is a multi-subunit chromatin remodeling complex that uses energy from ATP hydrolysis to reposition or eject nucleosomes at non-coding regulatory elements, thereby enabling access to the underlying DNA for transcriptional activation. Notably, the SWI/SNF complex plays a crucial role in chromatin remodeling and is recurrently altered in over 20% of human cancers, with the revised comple

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Xiao, Lanbo, Abhijit Parolia, Yuanyuan Qiao, et al. "Abstract 5469: Targeting SWI/SNF ATPases in enhancer-addicted prostate cancer." Cancer Research 82, no. 12_Supplement (2022): 5469. http://dx.doi.org/10.1158/1538-7445.am2022-5469.

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Abstract The switch/sucrose non-fermentable (SWI/SNF) complex plays a crucial role in chromatin remodeling and is recurrently altered in over 20% of human cancers. Here, we developed a proteolysis targeting chimera (PROTAC) degrader of ATPase subunits of the SWI/SNF complex, SMARCA2 and SMARCA4. Intriguingly, we found androgen receptor (AR)/forkhead box A1 (FOXA1)-positive prostate cancer to be exquisitely sensitive to dual SMARCA2 and SMARCA4 degradation relative to benign prostate as well as other cancer cell lines, including those with inactivating SMARCA4 mutations. Mechanistically, SWI/SN

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Hore, Pradipta, Sandipkumar Bambhaniya, and Murali Dharan Bashyam. "Abstract 264: The E3 ubiquitin ligase WWP2 regulates stability of the chromatin remodeler ARID1B." Cancer Research 85, no. 8_Supplement_1 (2025): 264. https://doi.org/10.1158/1538-7445.am2025-264.

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Abstract The Switch/sucrose-non-fermentable (SWI/SNF; also known as BRG1 associated factors (BAF)) chromatin remodeling complex functions to slide/evict nucleosomes thus making DNA available for multiple DNA-protein interactions to facilitate cardinal nuclear processes. Work during past two decades has revealed the cardinal role of the BAF complex in modulating tumorigenesis. ARID1B, a well-known tumor suppressor and a key subunit of the cBAF complex, is frequently mutated across various cancer types. Although the downregulation of ARID1B transcript levels has been observed in many cancers, ou

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Khosrowjerdi, Sara J., Nora K. Horick, Jeffrey William Clark, et al. "Clinical and mutational profile of ARID1A-mutated gastrointestinal cancers: Duration of response to platinum-based chemotherapy." Journal of Clinical Oncology 39, no. 15_suppl (2021): e15611-e15611. http://dx.doi.org/10.1200/jco.2021.39.15_suppl.e15611.

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e15611 Background: ARID1A is mutated in several cancer types, with studies reporting mutations in up to 10% of colorectal cancers (CRC) and as high as 35% of gastric and pancreatic cancers. The ARID1A gene encodes a member of the SWI/SNF (SWItch/Sucrose Non-Fermentable) chromatin remodeling complex and functions as a tumor suppressor. ARID1A has also been implicated in double-stranded DNA repair via both homologous recombination and non-homologous end-joining, potentially conferring platinum sensitivity. We sought to characterize this subset of gastrointestinal (GI) malignancies. Methods: We i

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Bajaj, Anubha. "Exiguous and Scarce-SMARCB1 Deficient Medullary Renal Cell Carcinoma." Cell & Cellular Life Sciences Journal 8, no. 2 (2023): 1–4. http://dx.doi.org/10.23880/cclsj-16000188.

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Switch / sucrose non fermentable (SWI/SNF) related, matrix associated, actin dependent regulator of chromatin subfamily B member 1 (SMARCB1) deficient medullary renal cell carcinoma is an exceptionally discerned, aggressive carcinoma associated with deficiency of SMARCB1 or integrase interactor 1(INI1).

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Ho, Rebecca, Bengul Gokbayrak, Eunice Li, et al. "Abstract 443: Targeting therapeutic vulnerabilities mediated by epigenetic reprogramming in ARID1A and ARID1B dual-deficient gynecologic cancers." Cancer Research 85, no. 8_Supplement_1 (2025): 443. https://doi.org/10.1158/1538-7445.am2025-443.

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Abstract Background: Dedifferentiated carcinoma of the uterus and the ovary (DDEC collectively) are rare gynecologic cancers made of low-grade differentiated adenocarcinoma of the uterus or ovary juxtaposed against undifferentiated carcinoma. The two components are clonally related, and previous studies have suggested that loss of various switch/sucrose non-fermentable (SWI/SNF) proteins may contribute to the transformation of differentiated cancer cells to an undifferentiated state. Specifically, a third of all DDECs have co-inactivation of cBAF-specific subunits ARID1A and ARID1B. cBAF is on

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Wedekind, Mary Frances, Srivandana Akshintala, Brigitte C. Widemann, et al. "Phase 1/2 study of tiragolumab and atezolizumab in patients with relapsed or refractory SMARCB1 or SMARCA4 deficient tumors." Journal of Clinical Oncology 41, no. 16_suppl (2023): TPS10066. http://dx.doi.org/10.1200/jco.2023.41.16_suppl.tps10066.

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TPS10066 Background: The SMARCB1/A4 gene products are core subunits of the SWItch/Sucrose Non-fermentable (SWI/SNF) chromatin remodeling complex. Tumors with defects in SWI/SNF are histologically distinct aggressive cancers occurring in children and young adults. SMARCB1/A4 deficient tumors, particularly rhabdoid tumors, poorly differentiated chordoma, epithelioid sarcoma, and medullary renal cell carcinoma, have immune cell infiltrates and programmed death ligand 1 (PD-L1) expression. Response to immune checkpoint inhibition (CI) has been observed in SMARCB1/A4 deficient tumors; however, resp

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Lin, Frank Po-Yen, Subotheni Thavaneswaran, Christine E. Napier, et al. "Genomic therapy matching in rare and refractory cancers: Updated results from a retrospective cohort study in the Molecular Screening and Therapeutic (MoST) program." Journal of Clinical Oncology 41, no. 16_suppl (2023): 1540. http://dx.doi.org/10.1200/jco.2023.41.16_suppl.1540.

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1540 Background: Biomarker actionability and therapy matching are two central concepts in precision oncology. However, the best strategy to align therapy with genomic alterations remains unclear. Here we report the updated results from a cohort study conducted in an Australian precision oncology program (MoST, ACTRN12616000908437), examining a therapy matching strategy based on comprehensive genomic profiling (CGP) results. Methods: All patients (pts) with rare or advanced solid tumours undergoing CGP from 2016 to 2021 after exhausting standard treatments were included. The primary outcome was

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