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Targeting the SWI/SNF complexes in POU2F transcription factor driven malignancies [ChIP-seq]

ABSTRACT: Targeting the SWI/SNF complexes in POU2F transcription factor driven malignancies [ChIP-seq]

PROVIDER: PRJNA1040957 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26846457_1.fastq.gz	Fastqsanger.gz
	SRR26846457_2.fastq.gz	Fastqsanger.gz
	SRR26846458_1.fastq.gz	Fastqsanger.gz
	SRR26846458_2.fastq.gz	Fastqsanger.gz
	SRR26846459_1.fastq.gz	Fastqsanger.gz

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Targeting the SWI/SNF complexes in POU2F transcription factor driven malignancies [RNA-seq]

Project description:The SWI/SNF chromatin-remodeling complex, pivotal in transcriptional regulation, has emerged as a significant player in tumorigenesis, unveiling therapeutic targeting prospects in specific malignancies. This investigation accentuates the potential of targeting the SWI/SNF complex in POU2F3-driven Small Cell Lung Cancer (SCLC) and POU2AF1-dependent multiple myelomas. Employing functional CRISPR screening and pharmacological validation, we identified a distinct and biased dependency of POU2F3-driven SCLC cells on the SWI/SNF complex. In vivo studies exhibited significant tumor growth inhibition in POU2F3-driven SCLC xenografts with an orally administered SMARCA2/4 PROTAC degrader. Furthermore, the exploration extended to POU2AF1 complex-dependent B-cell malignancies, revealing similar sensitivity to the SWI/SNF ATPase PROTAC degrader, suggesting a shared therapeutic potential in POU2F complex-driven malignancies. These collective findings highlight the SWI/SNF complex as a promising therapeutic target, catalyzing the advancement of innovative and efficacious treatment approaches to address these transcription factor-driven malignancies, addressing a critical medical challenge.

2024-02-15 | GSE247949 | GEO

Targeting the SWI/SNF complexes in POU2F transcription factor driven malignancies [ChIP-seq]

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Targeting the SWI/SNF complexes in POU2F transcription factor driven malignancies [ATAC-seq]

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Targeting the SWI/SNF complexes in POU2F transcription factor driven malignancies

Project description:Targeting the SWI/SNF complexes in POU2F transcription factor driven malignancies

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Targeting the SWI/SNF complexes in POU2F transcription factor driven malignancies [ATAC-seq]

Project description:Targeting the SWI/SNF complexes in POU2F transcription factor driven malignancies [ATAC-seq]

| PRJNA1040956 | ENA

Targeting the SWI/SNF complexes in POU2F transcription factor driven malignancies [RNA-seq]

Project description:Targeting the SWI/SNF complexes in POU2F transcription factor driven malignancies [RNA-seq]

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BCL7A-containing SWI/SNF/BAF complexes modulate mitochondrial bioenergetics during neural progenitor differentiation.

Project description:Mammalian SWI/SNF/BAF chromatin remodeling complexes influence cell lineage determination. While the contribution of mammalian SWI/SNF/BAF complexes in neural progenitor cell (NPC) proliferation and differentiation has been reported, little is known about the transcriptional profiles that determine neurogenesis or gliogenesis. Here we report that BCL7A is a modulator of the SWI/SNF/BAF complex and stimulates the genome-wide occupancy of the ATPase BRG1. We demonstrate that BCL7A is dispensable for SWI/SNF/BAF complex integrity, whereas it is essential to regulate Notch/Wnt pathway and mitochondrial bioenergetics in differentiating NPCs. Together, our findings uncover the unique mechanistic contribution of BCL7A-containing SWI/SNF/BAF complex in mitochondria-driven NPC commitment, thereby providing a better understanding of the cell-intrinsic transcriptional processes that connect metabolism, neuronal morphogenesis and cognitive flexibility.

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BCL7A-containing SWI/SNF/BAF complexes modulate mitochondrial bioenergetics during neural progenitor differentiation.

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BCL7A-containing SWI/SNF/BAF complexes modulate mitochondrial bioenergetics during neural progenitor differentiation.

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Organization, genomic targeting and assembly of three distinct SWI/SNF chromatin remodeling complexes in Arabidopsis [ChIP-seq]

Project description:Switch defective/sucrose non-fermentable (SWI/SNF) complexes are evolutionarily conserved multi-subunit machines that play vital roles in chromatin architecture regulation for modulating gene expression via sliding or ejection of nucleosomes in eukaryotes. In plants, perturbations of SWI/SNF subunits often result in severe developmental disorders. However, the subunit composition, pathways of assembly, and genomic targeting of the plant SWI/SNF complexes remain undefined. Here, we reveal that Arabidopsis SWI/SNF complexes exist in three distinct final form assemblies: BRM-associated SWI/SNF complexes (BAS), SYD-associated SWI/SNF complexes (SAS) and MINU-associated SWI/SNF complexes (MAS). We show that BAS complexes are equivalent to human ncBAF, whereas SAS and MAS complexes evolve in multiple subunits unique to plants, suggesting a plant-specific functional evolution of SWI/SNF complexes. We further demonstrate overlapping and specific genomic targeting of the three plant SWI/SNF complexes on chromatin and reveal that SAS complexes are necessary for the correct genomic localization of the BAS complexes. Finally, by focusing on the SAS and BAS complexes, we establish a requirement for both the core module subunit and the ATPase in the assembly of the plant SWI/SNF complexes. Together, our work highlights the divergence of SWI/SNF chromatin remodelers during the eukaryote evolution and provides a comprehensive landscape for understanding the plant SWI/SNF complexes organization, assembly, genomic targeting, and function.

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