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ATAC-seq of MUTZ3 cells in experiments to investigate EVI1 regulation

ABSTRACT: ATAC-seq of MUTZ3 cells in experiments to investigate EVI1 regulation

PROVIDER: PRJEB42211 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR5021521_1.fastq.gz	Fastqsanger.gz
	ERR5021521_2.fastq.gz	Fastqsanger.gz
	ERR5021522_1.fastq.gz	Fastqsanger.gz
	ERR5021522_2.fastq.gz	Fastqsanger.gz

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RNA-seq of MUTZ3 cells in experiments to investigate EVI1 regulation

Project description:RNA-seq of MUTZ3 cells in experiments to investigate EVI1 regulation

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ATAC-seq of MUTZ3 cells in experiments to investigate EVI1 regulation

Project description:Open chromatin regions were analyzed by ATAC-seq in MUTZ3 and MOLM1 cell lines (both inv(3) AML) to characterize the GATA2 super-enhancer region. ATAC-seq was performed as described (Buenrostro et al., 2013) with a modification in the lysis buffer to reduce mitochondrial DNA contamination.

2021-07-26 | E-MTAB-9949 | biostudies-arrayexpress

ChIP-seq of MUTZ3 cells in experiments to investigate EVI1 regulation by CRISPR or compound treatment

Project description:ChIP-seq of MUTZ3 cells in experiments to investigate EVI1 regulation by CRISPR or compound treatment

| PRJEB42227 | ENA

RNA-seq of MUTZ3 cells in experiments to investigate EVI1 regulation

Project description:We investigated whether GATA2 enhancer-driven transcription of EVI1 in inv(3)/t(3;3) is reversible in leukemia cells. In primary inv(3)/t(3;3) AML, immature CD34+CD15- cells can be discriminated from more mature CD34-CD15- and CD34-CD15+ cells. Besides, we also investigated the effect of deleting a MYB binding site on these cells using CRISPR/Cas9.

2021-07-26 | E-MTAB-9939 | biostudies-arrayexpress

ChIP-seq of MUTZ3 cells in experiments to investigate EVI1 regulation by CRISPR or compound treatment

Project description:ChIP-seq was conducted to evaluate the effect of deleting a MYB binding site in the GATA2 super-enhancer or treating MUTZ3 cells with a MYB inhibitor. H3K27ac, MYB and p300 ChIP-seq datasets were generated.

2021-07-26 | E-MTAB-9959 | biostudies-arrayexpress

Cut&Run-seq of MUTZ3 cells to investigate changes in a translocated enhancer following CRISPR treatment

Project description:We examined the effects of targeting the GATA2 super-enhancer on EVI1 expression in MUTZ3. To that end, we conducted genome editing with CRISPR and assessed H3K27 acetylation with Cut&Run. The protocol described by the Henikoff group was used to generate these data.

2021-07-26 | E-MTAB-9946 | biostudies-arrayexpress

Chromatin interactions of the EVI1 oncogene in myeloid leukaemia (ATAC-Seq)

Project description:EVI1 expression is associated with poor prognosis in myeloid leukaemia. Aberrant expression can result from Chr.3q alterations, which cause juxtaposition of enhancers that induce EVI1 activation via long-range chromatin interactions. More often, however, EVI1 expression occurs unrelated to 3q alterations, and it is unclear if its expression underlies similar dependencies as 3q+ cells. As enhancers regulate promoters by physical interaction/chromatin looping, we explored if the EVI1 promoter in EVI1+3q- cells interacts with distally located chromatin and if these intereactions promote EVI1 expression. To monitor TF binding sites at interactions involving active chromatin, we performed ATAC-Seq.

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EVI1 activates tumor-promoting transcriptional enhancers in pancreatic cancer [ATAC-seq].

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Project description:Acute myeloid leukemia (AML) driven by the activation of EVI1 due to chromosome 3q26/MECOM rearrangements is incurable with current chemotherapy regimens. Insight into the mechanism by which EVI1 drives myeloid transformation is needed to target EVI1 in those leukemias. Here we demonstrate recurrent interaction of CTBP1/2 with a unique PLDLS motif in EVI1, which is indispensable for leukemic transformation of 3q26/MECOM rearranged AML. A PLDLS competitor construct outcompetes EVI1 to CTBP1/2 binding and inhibits AML proliferation in xenotransplant models. This proof-of-concept study opens the possibility to target one of the most incurable forms of AML using specific inhibitors directed to EVI1/CTBP1/2 interaction. Our findings have important implications for other tumour types with aberrant expression of EVI1 or other oncogenic transcription factors that also depend on CTBP1/2 interaction.

2023-07-13 | PXD043333 | Pride

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