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

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE234203 | GEO | 2025/04/15

REPOSITORIES: GEO

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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

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

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

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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Expression profiling of Burkitt's lymphoma cells 24h after FOXM1 shRNA or MYB shRNA lentivirus-mediated transduction

Project description:Human Burkitt's lymphoma ST486 cells were transduced with non-target control shRNA lentiviral vectors, FOXM1 shRNA, and MYB shRNA lentiviral vectors. Total RNA was isolated 24h later. cRNA was produced with the standard one-step IVT protocol (Affymetix) and hybridized in U95Av2 gene chips (Affymetrix). Experiment consists in 3 independent samples: Expression profiling of Burkitt's lymphoma cells 24h after non-target control shRNA lentiviral mediated transduction. Expression profiling of Burkitt's lymphoma cells 24h after FOXM1 shRNA lentiviral mediated transduction. Expression profiling of Burkitt's lymphoma cells 24h after MYB shRNA lentiviral mediated transduction. Data processing performed using MAS5 or GCRMA.

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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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MYB-regulated pancreatic cancer secretome

Project description:Earlier we have shown important roles of MYB in pancreatic tumor pathobiology. To better understand the role of MYB in the tumor microenvironment and identify MYB-associated secreted biomarker proteins, we conducted mass spectrometry analysis of the secretome from MYB-modulated and control pancreatic cancer cell lines. We also performed in silico analyses to determine MYB-associated biofunctions, gene networks and altered biological pathways. We further investigated the secreted proteins for their potential biomarker properties.

2021-09-08 | PXD015126 | Pride

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