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

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

ORGANISM(S): Homo sapiens

PROVIDER: GSE234202 | 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)

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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

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

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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.

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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.

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MAZ induces MYB expression during the exit from quiescence via the E2F site in the MYB promoter

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Project description:The c-Myb transcription factor is highly expressed in immature hematopoietic cells and down-regulated during differentiation. To define the role of c-Myb in human hematopoietic lineage commitment, we studied the effects of its silencing during the commitment of human CD34+ Hematopoietic stem/progenitor cells. In CD34+ cells c-Myb silencing determined a cell cycle arrest in G0/G1 phase which strongly decreased the clonogenic efficiency, togheter with a reduction of erythroid colonies coupled with an increase of the macrophage and megakaryocyte ones. Moreover, morphological and flow cytometry data supported the preferential macrophage and megakaryocyte differentiation of c-Myb-silenced CD34+ cells. Taken together our data indicate that c-Myb is essential for the commitment along the erythroid and granulocyte lineages but not for the macrophage and megakaryocyte differentiation. Gene expression profiling of c-Myb-silenced CD34+ cells identified some potential c-Myb targets which can account for these effects, to study by Chromatin Immunoprecipitation and Luciferase Reporter Assay.

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