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

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

PROVIDER: PRJNA1040953 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26846520_1.fastq.gz	Fastqsanger.gz
	SRR26846520_2.fastq.gz	Fastqsanger.gz
	SRR26846521_1.fastq.gz	Fastqsanger.gz
	SRR26846521_2.fastq.gz	Fastqsanger.gz
	SRR26846522_1.fastq.gz	Fastqsanger.gz

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

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

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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 [RNA-seq]

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

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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]

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

Project description:Targeting the SWI/SNF complexes in POU2F transcription factor driven malignancies [ChIP-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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Project description:To comprehensively define the potential plant SWI/SNF sub-complexes and their subunits organization, we started by performing immuno-purification followed by mass spectrometry analysis (IP-MS) using stable transgenic Arabidopsis lines that expressed a green fluorescent protein (GFP)-tagged ATPase subunit, BRM (Li et al., 2016), SYD (Shu et al., 2021) or MINU2 (this study), driven by its native promoter in corresponding null mutant background.

2023-04-15 | PXD041567 |

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