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A lineage-specific super-enhancer for MYB controls the development of gastrointestinal adenocarcinomas

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE234204 | GEO | 2025/04/15

REPOSITORIES: GEO

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A lineage-specific super-enhancer for MYB controls the development of gastrointestinal adenocarcinomas (RNA-Seq)

Project description:To investigate the downstream target genes regulated by MYB, we performed gene expression profiling analysis in HT55 cells in which target gene has been knocked down by shRNA.

2025-04-15 | GSE234203 | GEO

A lineage-specific super-enhancer for MYB controls the development of gastrointestinal adenocarcinomas (ChIP-seq)

Project description:Chromatin immunoprecipitation DNA-sequencing (ChIP-seq) for MYB in HT55 cells.

2025-04-15 | GSE234202 | GEO

A lineage-specific super-enhancer for MYB controls the development of gastrointestinal adenocarcinomas

Project description:A lineage-specific super-enhancer for MYB controls the development of gastrointestinal adenocarcinomas

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Systemic genome-epigenome analysis captures a lineage-specific super-enhancer for MYB in gastrointestinal cancer

Project description:The gastrointestinal adenocarcinoma is a major cancer type for the digestive system, ranking as the top cause of cancer-related deaths worldwide. In contrast to the large body of studies on the mutations of protein-coding gene, the knowledge about the landscape of its non-coding regulatory elements is still insufficient. Combining the analysis of enhancer profiling and genomic structural variation, we discovered and validated a lineage-specific super-enhancer for MYB in gastrointestinal adenocarcinoma. This super-enhancer is constituted by a predominant enhancer e4 and multiple facilitator enhancers, whose transcriptional activity is controlled by the direct binding of HNF4A and MYB itself. Suppression of the super-enhancer downregulated the expression of MYB, inhibited the downstream Notch signaling and prevented the development of gastrointestinal adenocarcinoma in vitro and in vivo. Our study revealed a novel regulatory mechanism activating MYB expression in a lineage-specific manner, which provided an inspiring insight into the carcinogenic mechanism and therapeutic strategies for gastrointestinal adenocarcinoma.

| S-SCDT-10_1038-S44320-025-00098-1 | biostudies-other

A lineage-specific super-enhancer for MYB controls the development of gastrointestinal adenocarcinomas (ChIP-seq)

Project description:A lineage-specific super-enhancer for MYB controls the development of gastrointestinal adenocarcinomas (ChIP-seq)

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A lineage-specific super-enhancer for MYB controls the development of gastrointestinal adenocarcinomas (RNA-Seq)

Project description:A lineage-specific super-enhancer for MYB controls the development of gastrointestinal adenocarcinomas (RNA-Seq)

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Lineage-specific RUNX2 super-enhancer activates MYC and promotes the development of blastic plasmacytoid dendritic cell neoplasm.

Project description:Blastic plasmacytoid dendritic cell neoplasm (BPDCN) is an aggressive subtype of acute leukemia, the cell of origin of which is considered to be precursors of plasmacytoid dendritic cells (pDCs). Since translocation (6;8)(p21;q24) is a recurrent anomaly for BPDCN, we demonstrate that a pDC-specific super-enhancer of RUNX2 is associated with the MYC promoter due to t(6;8). RUNX2 ensures the expression of pDC-signature genes in leukemic cells, but also confers survival and proliferative properties in BPDCN cells. Furthermore, the pDC-specific RUNX2 super-enhancer is hijacked to activate MYC in addition to RUNX2 expression, thereby promoting the proliferation of BPDCN. We also demonstrate that the transduction of MYC and RUNX2 is sufficient to initiate the transformation of BPDCN in mice lacking Tet2 and Tp53, providing a model that accurately recapitulates the aggressive human disease and gives an insight into the molecular mechanisms underlying the pathogenesis of BPDCN.

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Progressing super-enhancer landscape during mammary differentiation controls tissue-specific gene regulation.

Project description:The mammary luminal lineage relies on the common cytokine-sensing transcription factor STAT5 to establish super-enhancers during pregnancy and initiate a genetic program that activates milk production. As pups grow, the greatly increasing demand for milk requires progressive differentiation of mammary cells with advancing lactation. Here we investigate how persistent hormonal exposure during lactation shapes an evolving enhancer landscape and impacts the biology of mammary cells. Employing ChIP-seq, we uncover a changing transcription factor occupancy at mammary enhancers, suggesting that their activities evolve with advancing differentiation. Using mouse genetics, we demonstrate that the functions of individual enhancers within the Wap super-enhancer evolve as lactation progresses. Most profoundly, a seed enhancer, which is mandatory for the activation of the Wap super-enhancer during pregnancy, is not required during lactation, suggesting compensatory flexibility. Combinatorial deletions of structurally equivalent constituent enhancers demonstrated differentiation-specific compensatory activities during lactation. We also demonstrate that the Wap super-enhancer, which is built on STAT5 and other common transcription factors, retains its exquisite mammary specificity when placed into globally permissive chromatin, suggesting a limited role of chromatin in controlling cell specificity. Our studies unveil a previously unrecognized progressive enhancer landscape where structurally equivalent components serve unique and differentiation-specific functions.

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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.

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Lineage-Specific Epigenomic and Genomic Activation of Oncogene HNF4A Promotes Gastrointestinal Adenocarcinomas

Project description:We profiled fresh-frozen esophageal tumor and normal samples and cell lines with chromatin immunoprecipitation sequencing (ChIP-Seq). Mathematically modeling was performed to establish (super)-enhancers landscapes and inter-connected transcriptional circuitry formed by master TFs. Coregulation and cooperation between master TFs was investigated by ChIP-Seq, RNASeq, 4C-Seq and luciferase assay. Biological functions of candidate factors were evaluated by measuring cell proliferation, colony formation, cell apoptosis and xenograft growth. Next-generation sequencing (NGS) has revolutionized systems-based analysis of cellular pathways. Here, we aim to compare of Eso26 cells knock down HNF4A with siRNA and control transcriptome profiling (RNA-seq) to microarray and quantitative reverse transcription polymerase chain reaction (qRT–PCR) methods and to evaluate protocols for optimal high-throughput data analysis. We also report the application of circular chromatin conformation capture (4C) sequencing technology for studying master transcription factor (HNF4A) in human esophageal adenocarcinoma cancer cell lines (Eso26).

2020-06-14 | GSE132813 | GEO

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