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

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

PROVIDER: PRJNA980283 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24830779_1.fastq.gz	Fastqsanger.gz
	SRR24830779_2.fastq.gz	Fastqsanger.gz
	SRR24830780_1.fastq.gz	Fastqsanger.gz
	SRR24830780_2.fastq.gz	Fastqsanger.gz
	SRR24830781_1.fastq.gz	Fastqsanger.gz

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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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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 (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 (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

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

2025-04-15 | GSE234204 | GEO

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

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

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

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

| PRJNA549160 | ENA

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 cell’s 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.

2014-11-13 | GSE59657 | GEO

Bidirectional enhancer RNAs regulate different MYB promoters

Project description:MYB is a pivotal oncogenic driver in leukemia and is overexpressed through various mechanisms. Transcriptional regulation of MYB is complex with an alternative MYB promoter (TSS2) located in intron 1. Here, we identified two bidirectional enhancer RNAs transcribed from the -34 kb enhancer of MYB. These two eRNAs both upregulate MYB transcription, and promote proliferation and migration in leukemia cells. To further elucidate how eRNAs regulate MYB expression, we analyzed MYB differential exon usage in RNASeq data with the DEXSeq package after overexpression of eRNAs in K562 cells. We found that bidirectional enhancer RNAs regulate different MYB promoters. Transcription initiating from TSS2 produces N-terminally truncated MYB protein lacking the first 20 amino acids. To analyze the genes and pathways affected by both MYB isoforms, RNA-seq was performed after MYB or N-terminally truncated MYB was overexpressed in K562 cells. We found that N-terminally truncated MYB exhibits different activity in K562 cells, where it not only activates different primary targets, but also different downstream pathways altogether.

2024-08-01 | GSE263511 | GEO

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