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Genome-wde mapping of BRD9 binding sites and gene expression changes upon BRD9 knockdown

ABSTRACT: Genome-wde mapping of BRD9 binding sites and gene expression changes upon BRD9 knockdown

PROVIDER: PRJNA531322 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8863350_1.fastq.gz	Fastqsanger.gz
	SRR8863350_2.fastq.gz	Fastqsanger.gz
	SRR8863351_1.fastq.gz	Fastqsanger.gz
	SRR8863351_2.fastq.gz	Fastqsanger.gz
	SRR8863346_1.fastq.gz	Fastqsanger.gz

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Genome-wde mapping of BRD9 binding sites and gene expression changes upon BRD9 knockdown

Project description:Leukemia is characterized by genetic and epigenetic mutations resulting in selection of cancer cells, which are unable to differentiate. While genetic alterations are difficult to target, the epigenome is intrinsically dynamic and readily offers new therapeutic strategies. Thus, identifying cancer-specific context-dependent targets and unraveling their biological function may open up new therapeutic perspectives. Here, we identify bromodomain-containing protein 9 (BRD9) as a critical target required in acute myeloid leukemia (AML). We show that BRD9 is overexpressed in AML cells including ex vivo primary blasts compared to CD34+ cells. By targeting BRD9 expression in AML, we observed an alteration in proliferation and survival, ultimately resulting in the induction of apoptosis. Intriguingly, genome-wide profiling revealed that BRD9 binds enhancer regions in a cell type-specific manner, regulating cell type-related processes. We unveil a novel BRD9-sustained STAT5 pathway activation via regulation of SOCS3 expression levels. Our findings identify a previously undescribed BRD9-STAT5 axis as critical for leukemia maintenance, suggesting BRD9 as a potential therapeutic target.

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HNF4G, AR, FOXA1, H3K4me1, H3K27acetyl binding sites upon knockdown and overexpression of HNF4G in 22Rv1 and LNCaP prostate cancer cells respectively

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Project description:We performed RNA-seq to investigate global changes in gene expression in proliferating myoblasts transduced with either the scramble, Baf250A, Brd9 or Baf180 shRNAs. This study revelaed that the Baf250-containing BAF complex and the Brd9-containing ncBAF complex contribute to myoblast proliferation but the Baf180-containing PBAF subfamily does not.

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The role of GABPA,GPD1L and BRD9 in renal cancer progression and metasasis

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Transcriptome changes upon Cas13-based knockdown

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Project description:Genes encoding subunits of SWI/SNF (BAF) chromatin remodeling complexes are mutated in >20% of cancers. SWI/SNF complexes exist in three distinct families that each contribute to regulation of transcription, although the functional interactions between the families are not well understood. Rhabdoid tumors constitute an informative model system as these highly aggressive cancers are driven by inactivation of a single SWI/SNF subunit, SMARCB1, which is present in two SWI/SNF families (cBAF and PBAF) but not in the third (GBAF/ncBAF). We and others have shown that BRD9, a therapeutically targetable member of ncBAF, is essential specifically in SMARCB1-deficient cancers, suggesting key functional relationships between SMARCB1-containing complexes and BRD9/ncBAF. However, the mechanistic underpinnings of these relationships are poorly understood. Here, we demonstrate that genomic binding of BRD9 is largely dependent upon SMARCB1 such that the absence of SMARCB1 results in significantly reduced BRD9 binding. At select sites, however, we show that SMARCB1-loss results in gain of BRD9 binding and BRD9-dependent accessibility. We find that this gain is associated with expression of genes promoting cell migration. Our results define relationships between SWI/SNF complex families, elucidate mechanisms by which SMARCB1 loss drives oncogenesis, and provide mechanistic insight into the synthetic-lethal relationship between SMARCB1 and BRD9.

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Functional interplay between SWI/SNF complexes underlies BRD9 dependency in SMARCB1-mutant cancers [ATAC-seq]

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