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EVI1 activates tumor-promoting transcriptional enhancers in pancreatic cancer.

ABSTRACT: EVI1 activates tumor-promoting transcriptional enhancers in pancreatic cancer.

PROVIDER: PRJNA701163 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13675100.fastq.gz	Fastqsanger.gz
	SRR13675101.fastq.gz	Fastqsanger.gz
	SRR13675102.fastq.gz	Fastqsanger.gz
	SRR13675103.fastq.gz	Fastqsanger.gz
	SRR13675104.fastq.gz	Fastqsanger.gz

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

Project description:EVI1 activates tumor-promoting transcriptional enhancers in pancreatic cancer [RNA-seq].

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

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

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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.

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

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

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EVI1 activates tumor-promoting transcriptional enhancers in pancreatic cancer.

Project description:Cancer cells utilize epigenetic alterations to acquire autonomous capabilities for tumor maintenance. Here, we show that pancreatic ductal adenocarcinoma (PDA) cells utilize super-enhancers (SEs) to activate the transcription factor EVI1 (ecotropic viral integration site 1) gene, resulting in activation of an EVI1-dependent transcription program conferring PDA tumorigenesis. Our data indicate that SE is the vital cis-acting element to maintain aberrant EVI1 transcription in PDA cells. Consistent with disease progression and inferior survival outcomes of PDA patients, we further show that EVI1 upregulation is a major cause of aggressive tumor phenotypes. Specifically, EVI1 promotes anchorage-independent growth and motility in vitro and enhances tumor propagation in vivo. Mechanistically, EVI1-dependent activation of tumor-promoting gene expression programs through the stepwise configuration of the active enhancer chromatin attributes to these phenotypes. In sum, our findings support the premise that EVI1 is a crucial driver of oncogenic transcription programs in PDA cells. Further, we emphasize the instructive role of epigenetic aberrancy in establishing PDA tumorigenesis.

| S-EPMC8210884 | biostudies-literature

EVI1 activates tumor-promoting transcriptional enhancers in pancreatic cancer.

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

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Chromatin interactions of the EVI1 oncogene in myeloid leukaemia (4C-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.

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

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