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Shared requirement for MYC upstream super-enhancer region in tissue regeneration and cancer

ABSTRACT: Shared requirement for MYC upstream super-enhancer region in tissue regeneration and cancer

PROVIDER: PRJNA1022134 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26213423.fastq.gz	Fastqsanger.gz
	SRR26213424.fastq.gz	Fastqsanger.gz
	SRR26213425.fastq.gz	Fastqsanger.gz
	SRR26213426.fastq.gz	Fastqsanger.gz
	SRR26213427.fastq.gz	Fastqsanger.gz

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Shared requirement for MYC upstream super-enhancer region in tissue regeneration and cancer

Project description:Cancer has been characterized as a wound that does not heal. Malignant cells are morphologically distinct from normal proliferating cells but have extensive similarities to tissues undergoing wound healing and/or regeneration. The mechanistic basis of this similarity has, however, remained enigmatic. Here we show that the genomic region upstream of Myc, which is required for intestinal tumorigenesis, is also required for intestinal regeneration after radiation damage. The region is also critical for growth of adult intestinal cells in 3-D organoid culture, indicating that culture conditions that recapitulate most aspects of normal tissue architecture still reprogram normal cells to proliferate using a mechanism similar to that employed by cancer cells. Our results uncover a genetic link between tissue regeneration and tumorigenesis, and establish that normal tissue renewal and regeneration of tissues after severe damage are mechanistically distinct.

2025-03-30 | GSE244298 | GEO

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Project description:Shared requirement for MYC upstream super-enhancer in tissue regeneration and cancer

| PRJEB57218 | ENA

Requirement for the Mediator kinase module for activation of super-enhancer associated genes in colon cancer cells

Project description:RNA sequencing of HCT116 colon cancer cells following single and combined depletions of Mediator kinase module subunits CDK8, CDK19, MED12, MED13 and MED13L and the BET family protein BRD4. The results provide insight into the shared and specific functions of kinase module subunits and BRD4 in regulation of expression of transcriptional programs including genes associated with cancer acquired super-enhancers.

2018-04-02 | E-MTAB-5873 | biostudies-arrayexpress

Chromatin interactions involving super-enhancers associate with specific expression patterns of target genes

Project description:Super-enhancers may regulate target genes through chromatin looping. We connected super-enhancers in the K562 chronic myelogenous leukemia cell line with chromatin interactions identified from Chromatin Interaction Analysis with Paired-End Tag (ChIA-PET) data. Gene expression at proximal elements that are connected with distal super-enhancers showed significantly higher cell-type specificity than at proximal elements connected with other elements or not involved in interaction. 4C and Episwitch analysis of chromatin interactions showed that certain chromatin interactions are cell-specific, but others are more general. While super-enhancers upstream of c-MYC at the MYC-335 element can be found in other cancers, only super-enhancers downstream of c-MYC can be found in K562. 4C analysis of the c-MYC promoter revealed no chromatin interactions that are directed upstream of c-MYC, but only downstream of c-MYC, in the PVT1 long non-coding RNA gene. Cell-specific usage of super-enhancers could explain why the MYC-335 element that is associated with many solid cancers such as colorectal cancer and breast cancer, but not with leukemia. Surprisingly, we found that a chromatin interaction between c-MYC and a c-MYC super-enhancer is lost in chronic myelogenous leukemia patient blood as compared with blood from individuals without the disease through Oxford Biodynamicsâ?? Episwitch analysis. These results provide evidence for fine-tuning of expression patterns, such as cell-specific regulation of target genes by distal super-enhancers through chromatin interactions and an association between chromatin interactions and disease, and highlight that super-enhancers are more complex than previously described. Examination of several chromatin interactions involving super-enhancers using 4C-Seq and Episwitch (TM)

2017-05-01 | E-GEOD-77125 | biostudies-arrayexpress

Improved Super-Resolution Ribosome Profiling Reveals Prevalent Translation of Upstream ORFs and Small ORFs in Arabidopsis

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Requirement for TP73 in cancer cell maintenance and genetic alterations originating from its intragenic super-enhancer

Project description:Requirement for TP73 in cancer cell maintenance and genetic alterations originating from its intragenic super-enhancer

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Requirement for the Mediator kinase module for activation of super-enhancer associated genes in colon cancer cells

Project description:Requirement for the Mediator kinase module for activation of super-enhancer associated genes in colon cancer cells

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An Oncogenic Super-Enhancer Formed through Somatic Mutation of a Noncoding Intergenic Element

Project description:In many cancers, critical oncogenes are driven from large regulatory elements, called super-enhancers, which recruit much of the cellM-bM-^@M-^Ys transcriptional apparatus and are defined by extensive H3K27 acetylation. We found that in T-cell acute lymphoblastic leukemia (T-ALL), somatic heterozygous mutations introduce MYB binding motifs in a precise noncoding site, which nucleate a super-enhancer upstream of the TAL1 oncogene. Further analysis of genome-wide binding identified MYB and its histone acetylase binding partner CBP as core components of the TAL1 complex and of the TAL1-mediated feed-forward auto-regulatory loop that drives T-ALL. Furthermore, MYB and CBP occupy endogenous MYB binding sites in the majority of super-enhancer sites found in T-ALL cells. Thus, our study reveals a new mechanism for the generation of super-enhancers in malignant cells involving the introduction of somatic indel mutations within non-coding sequences, which introduce aberrant binding sites for the MYB master transcription factor. ChIP-Seq for transcription factors and co-factors in T cell acute lymphoblastic leukemia cell lines

2014-11-13 | E-GEOD-59657 | biostudies-arrayexpress

Suppression of oncogenic super enhancers in MYC-dependent AMLs by NR4A Nuclear Receptors

Project description:NR4A nuclear receptors are tumor suppressors of acute myeloid leukemia (AML) that are silenced in AML at the level of transcription elongation. Using RNA-Seq, we show that NR4As inhibit leukemic cell growth largely through suppression of MYC pathway genes. MYC is highly expressed in AML and contributes to AML progression and therapeutic resistance. MYC expression in AML is driven by a super enhancer cluster 1.8Mbp downstream of the MYC locus, which is highly sensitive to therapeutic intervention, including treatment with BET inhibitors. We recently identified dihydroergotamine (DHE) as an FDA-approved drug that strongly induces NR4A transcription in AML cells and operates effectively as an antileukemic therapy. RNA-Seq in MOLM-14 identified MYC as the most statistically repressed target of DHE. Using ChIP-Seq for MED1 as a readout for Mediator occupancy, we identified super enhancers in MOLM-14 cells and show that treatment with DHE significantly suppresses MED1 signal across a subset of super enhancers, including the MYC super enhancer. Finally, we demonstrate that NR4As are broadly associated with global super enhancers, including sites where super enhancer activity is retained, reduced, or gained.

2020-01-11 | GSE124963 | GEO

Distinct use of super-enhancer elements controls cell type-specific CD25 transcription and function

Project description:The IL-2 receptor α chain (IL-2Rα/CD25) is constitutively expressed on double-negative (DN2/DN3 thymocytes and regulatory T cells (Tregs) but induced by IL-2 on T and natural killer (NK) cells, with Il2ra expression regulated by a STAT5-dependent super-enhancer. We investigated CD25 regulation and function using a series of mice with deletions spanning STAT5-binding elements. Deleting the upstream super-enhancer region mainly affected constitutive CD25 expression on DN2/DN3 thymocytes and Tregs, with these mice developing autoimmune alopecia, whereas deleting an intronic region decreased IL-2-induced CD25 on peripheral T and NK cells. Thus, distinct super-enhancer elements preferentially control constitutive versus inducible expression in a cell type-specific manner. The mediator-1 coactivator colocalized with specific STAT5-binding sites. Moreover, both upstream and intronic regions had extensive chromatin interactions, and deletion of either region altered the super-enhancer structure in mature T cells. These results demonstrate differential functions for distinct super-enhancer elements, thereby indicating previously unknown ways to manipulate CD25 expression in a cell type-specific fashion.

2024-12-03 | GSE283392 | GEO

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