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

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

PROVIDER: PRJEB42227 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR5022160_1.fastq.gz	Fastqsanger.gz
	ERR5022160_2.fastq.gz	Fastqsanger.gz
	ERR5022161_1.fastq.gz	Fastqsanger.gz
	ERR5022161_2.fastq.gz	Fastqsanger.gz
	ERR5022162_1.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

| PRJEB42200 | ENA

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

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

| PRJEB42211 | ENA

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

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

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

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

ChIP-seq for the identification of enhancer and super enhancers in Acute Myeloid Leukemia cells with a 3q-aberration

Project description:To infer enhancers and super enhancers in Acute Myeloid Leukemia (AML) Cell lines with a 3q-aberration we determined regions enriched for H3K27AC, H3K4ME3, H3K4ME1, P300, and BRD4 in MOLM1. Additionally we determined regions enriched for P300 and BRD4 in the cell line Mutz3 which also harbors a 3q-aberration. As an control we performed Chip-Seq to determine enrichment for BRD4 in K562, which overexpresses the proto-oncogene EVI1, but has no apparent 3q-aberration. Ultimately, the ChipSeq experiments were utilized to infer which enhancer or super enhancer drives the overexpression of EVI1 in AMLs with a 3q-aberration. Finally, the effect of the compound JQ1 on the inferred super enhancers and the overexpression of EVI1 is tested by treating the cell line MOLM1 for 6 hours and determining the residual binding of BRD4.

2014-04-03 | E-MTAB-2224 | biostudies-arrayexpress

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

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

| PRJEB42209 | ENA

Effects of EVI1 and EVI1?324 mild expression in HeLa cells

Project description:We studied the variations of mRNA amounts after Flag-EVI1, Flag-EVI1?324, or Flag expression in HeLa cells. Despites EVI1 discovery in 1988, its recognized role as a dominant oncogene in myeloid leukemia and more recently in epithelial cancers, only a few target genes were known and it was not clear why EVI1 was involved in cancer progression. Here we obtained the genomic binding occupancy and expression data for EVI1 in human cells. We identified numerous EVI1 target cancer genes and genes controlling cell migration and adhesion. Moreover, we characterized a transcriptional cooperation between AP1 and EVI1 that regulated proliferation and adhesion through a feed-forward loop. This study provides human genome-wide mapping and expression analyses for EVI1 that will be useful for the research community. 12 samples were collected. Each condition was done in 4 replicates, collected 24 hours after transfection (for mild expression of EVI1 or EVI1?324). Transfections with Flag-expressing vector were used as controls.

2012-11-14 | E-GEOD-42251 | biostudies-arrayexpress

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

Project description:Cancer cells utilize epigenetic alterations to acquire autonomous capabilities for tumor maintenance. Here, we show that pancreatic ductal adenocarcinoma (PDA) cells hijack super-enhancers (SEs) to activate the EVI1 gene with its tumor-intrinsic program. We demonstrate that SE is the vital cis-acting element to maintain aberrant EVI1 transcription in PDA cells. Related to disease progression and inferior survival outcomes in human PDA, functional experiments further show that EVI1 upregulation is the cause of aggressive tumor phenotypes. In particular, EVI1 mediates the resistance to anchorage-independent growth and enhanced motility in vitro, with efficient tumor propagation in vivo. EVI1-dependent activation of gene expression program attributes to these phenotypes, by which EVI1 drives the stepwise configuration of the active enhancer chromatin. In sum, our findings support the promise that EVI1 is a crucial driver of oncogenic transcription program in PDA cells. Further, we emphasize the instructive role of epigenetic aberrancy in establishing PDA tumorigenesis.

2021-05-20 | GSE166510 | GEO

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