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Cistrome analysis of SKI and RUNX1 in HL60

ABSTRACT: Cistrome analysis of SKI and RUNX1 in HL60

PROVIDER: PRJNA420513 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6335160.fastq.gz	Fastqsanger.gz
	SRR6335170.fastq.gz	Fastqsanger.gz
	SRR6335180.fastq.gz	Fastqsanger.gz
	SRR6335161.fastq.gz	Fastqsanger.gz
	SRR6335171.fastq.gz	Fastqsanger.gz

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Cistrome analysis of SKI and RUNX1 in HL60

Project description:SKI is a transcriptional co-regulator and overexpressed in various human tumors, for example in acute myeloid leukemia (AML). SKI contributes to the origin and maintenance of the leukemic phenotype. Here we use ChIP-seq and RNA-seq to identify the epigenetic alterations induced by SKI overexpression in AML cells. We show that approximately two thirds of differentially expressed genes are up-regulated upon SKI deletion, of which nearly 50% harbour SKI binding sites in their proximity, primarily in enhancer regions. Gene ontology analysis reveals that many of the differentially expressed genes are annotated to hematopoietic cell differentiation and inflammatory response, corroborating our finding that SKI deletion causes a release of the myeloid differentiation block in HL60 cells. We find that SKI peaks are enriched for RUNX1 consensus motifs, particularly in up-regulated SKI targets. RUNX1 ChIP-seq demonstrates that nearly 70% of RUNX1 binding sites overlap with SKI peaks, mainly at enhancer regions. SKI and RUNX1 co-occupy the same genomic sites and cooperate in gene silencing. Our work demonstrates for the first time on a genome-wide scale the predominant co-repressive function of SKI in AML cells and uncovers the transcription factor RUNX1 as an important mediator of SKI-dependent transcriptional repression.

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Transcriptome analysis of SKI knock-out in HL60 cells

Project description:Whole transcriptome for SKI knock-out and control HL60 cells was sequenced. SKI control and knockout samples were compared to find differentially expressed genes. Differentially expressed genes were further analysed to find the significance of SKI in HL60 cells.

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Combined cistrome and transcriptome analysis of SKI in AML cells identifies SKI as a co-repressor for RUNX1

Project description:Combined cistrome and transcriptome analysis of SKI in AML cells identifies SKI as a co-repressor for RUNX1

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Transcriptome analysis of SKI knock-out in HL60 cells

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Combined cistrome and transcriptome analysis of SKI in AML cells identifies SKI as a co-repressor for RUNX1.

Project description:SKI is a transcriptional co-regulator and overexpressed in various human tumors, for example in acute myeloid leukemia (AML). SKI contributes to the origin and maintenance of the leukemic phenotype. Here, we use ChIP-seq and RNA-seq analysis to identify the epigenetic alterations induced by SKI overexpression in AML cells. We show that approximately two thirds of differentially expressed genes are up-regulated upon SKI deletion, of which >40% harbor SKI binding sites in their proximity, primarily in enhancer regions. Gene ontology analysis reveals that many of the differentially expressed genes are annotated to hematopoietic cell differentiation and inflammatory response, corroborating our finding that SKI contributes to a myeloid differentiation block in HL60 cells. We find that SKI peaks are enriched for RUNX1 consensus motifs, particularly in up-regulated SKI targets upon SKI deletion. RUNX1 ChIP-seq displays that nearly 70% of RUNX1 binding sites overlap with SKI peaks, mainly at enhancer regions. SKI and RUNX1 occupy the same genomic sites and cooperate in gene silencing. Our work demonstrates for the first time the predominant co-repressive function of SKI in AML cells on a genome-wide scale and uncovers the transcription factor RUNX1 as an important mediator of SKI-dependent transcriptional repression.

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Combined cistrome and transcriptome analysis of SKI in AML cells identifies SKI as a co-repressor for RUNX1

Project description:This SuperSeries is composed of the SubSeries listed below.

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Project description:While c-Src is infrequently mutated in human cancers, it mediates oncogenic signals of many activated growth factor receptors and thus remains a key potential target of cancer therapy. However, the widespread function of Src in many cell types and processes requires evaluation of Src-targeted therapeutics within a normal developmental and immune competent environment. In an effort to direct clinical use of Src inhibitors, we tested the effectiveness of one of the four Src inhibitors in clinical testing, SKI-606 (bosutinib), in the MMTV-PyVmT transgenic mouse model of breast cancer. Tumor formation in this model is dependent on the presence of Src, but the necessity of Src kinase activity for tumor formation has not been determined. Furthermore, Src inhibitors have not been examined in an autochthonous tumor model. Here we show that oral administration of the Src inhibitor SKI-606 inhibited the phosphorylation of Src in mammary tumors, and caused a rapid decrease in the Ezh2 Polycomb group histone H3K27 methyltransferase and an increase in epithelial organization. SKI-606 prevented the appearance of palpable tumors in more than half of the animals treated from puberty and stopped tumor growth in older animals with preexisting tumors. These antitumor effects were accompanied by decreased cellular proliferation, altered tumor blood vessel organization and dramatically increased differentiation to lactational and epidermal cell fates. SKI-606 controls the development of mammary tumors in this model by inducing differentiation. Differentiation of Mammary Tumors by SKI-606 (bostutinib)

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