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TCF4 is a key mediator of cell identity in neuroblastoma and vulnerable to protein degradation by multiple epigenetic factors [ChIP-seq]

ABSTRACT: TCF4 is a key mediator of cell identity in neuroblastoma and vulnerable to protein degradation by multiple epigenetic factors [ChIP-seq]

PROVIDER: PRJNA918614 | ENA |

REPOSITORIES: ENA

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TCF4 is a key mediator of cell identity in neuroblastoma and vulnerable to protein degradation by multiple epigenetic factors

Project description:TCF4 is a key mediator of cell identity in neuroblastoma and vulnerable to protein degradation by multiple epigenetic factors

| PRJNA918609 | ENA

TCF4 is a key mediator of cell identity in neuroblastoma and vulnerable to protein degradation by multiple epigenetic factors [RNA-seq]

Project description:TCF4 is a key mediator of cell identity in neuroblastoma and vulnerable to protein degradation by multiple epigenetic factors [RNA-seq]

| PRJNA918612 | ENA

TCF4 is a key mediator of cell identity in neuroblastoma and vulnerable to protein degradation by multiple epigenetic factors [ChIP-seq]

Project description:Neuroblastomas (NBs) are aggressive pediatric tumors that are responsible for up to 15% of all pediatric cancer deaths. Two differentiation states exist in NB tumors, a majority of more committed ADRN tumor cells and a minority of neural crest cell (MES/NCC)-like cells. The transition between identity states is governed by different sets of master TFs that collectively form core regulatory circuitries (CRC) that drive high expression of downstream lineage-specific genes. In this study we aim to discover new lineage dependency factors in NB. Here, we identified the E-box transcription factor TCF4 (E2-2) not previously reported in NB to be a critical factor shared across both NB states and play important role in driving NB oncogenesis. We performed multiple functional and high-throughput analysis to delineate the unrecognized function of TCF4 in NB

2024-08-05 | GSE222213 | GEO

TCF4 is a key mediator of cell identity in neuroblastoma and vulnerable to protein degradation by multiple epigenetic factors [RNA-seq]

2024-08-05 | GSE222212 | GEO

TCF4 is a key mediator of cell identity in neuroblastoma and vulnerable to protein degradation by multiple epigenetic factors

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

2024-08-05 | GSE222214 | GEO

Occupancy profiling of HAND2, MEIS2 and TCF4 by CUT&Tag from Neuroblastoma cells

Project description:HAND2, MEIS2 and TCF4 are master transcription factors (TFs) in neuroblastoma and create an interconnected core regulatory circuitry (CRC) by directly occupying each other's and their own super-enhancers (SEs), which leads to high levels of each TF expression inside the CRC. Additionally, CRC TFs cooperatively co-occupy the same SE components, which promotes the expression of genes involved in cell identity and cell-type-specific activities. Super-enhancer-mediated CRC enriched at key oncogenes in neuroblastoma. In the present study, CUT&Tag (Cleavage Under Targets and Tagmentation) analysis was performed to explore the target of HAND2, MEIS2 and TCF4 in NB cells.

2024-05-06 | GSE234337 | GEO

Mediator complex interaction partners organize the transcriptional network that defines neural stem cells

Project description:Mediator complex regulates transcription by connecting enhancers to promoters. High Mediator binding density defines super enhancers, which regulate cell-identity genes and oncogenes. Protein interactions of Mediator may explain its role in these processes but have not been identified comprehensively. Here we purify Mediator from neural stem cells (NSCs) and identify 75 protein-protein interaction partners. We identify super enhancers in NSCs and show that Mediator-interacting chromatin modifiers colocalise with Mediator at enhancers and super enhancers. Transcription factor families with high affinity for Mediator dominate enhancers and super enhancers and can explain genome-wide Mediator localization. We identify E-box transcription factor Tcf4 as a key regulator of NSCs. Tcf4 interacts with Mediator, colocalises with Mediator at super enhancers and regulates neurogenic transcription factor genes with super enhancers and broad H3K4me3 domains. Our data suggest that high binding-affinity for Mediator is an important organizing feature in the transcriptional network that determines NSC identity.

2019-05-06 | PXD013546 | Pride

Occupancy profiling of HAND2, MEIS2 and TCF4 by CUT&Tag from Neuroblastoma cells

Project description:Occupancy profiling of HAND2, MEIS2 and TCF4 by CUT&Tag from Neuroblastoma cells

| PRJNA981072 | ENA

Mediator complex interaction partners organize the transcriptional network that defines neural stem cells

Project description:The Mediator complex regulates transcription by connecting enhancers to promoters. High Mediator binding density is one defining feature of so-called super enhancers, which regulate cell-identity genes and oncogenes. Protein interactions of Mediator may explain its role in these processes but have not been identified comprehensively. Here we purify Mediator from neural stem cells (NSCs) and identify 77 novel protein-protein interaction partners. We identified super enhancers in NSCs and show that Mediator-interacting chromatin modifiers colocalise with Mediator at enhancers and super enhancers. Three transcription factor families with high affinity for Mediator dominate enhancers and super enhancers in NSCs and can explain genome-wide Mediator localization. We identify E-box transcription factor Tcf4 as a key regulator in NSCs. Tcf4 interacts with Mediator, colocalises and correlates with Mediator at super enhancers and regulates other neural transcription factors via super enhancers. Our data suggest that high binding-affinity for Mediator is an important organizing feature in the transcriptional network that determines NSC identity.

2019-04-01 | GSE109043 | GEO

Knockdown of human TCF4 affects multiple signaling pathways involved in cell survival, epithelial-to-mesenchymal transition and neuronal differentiation

Project description:TCF4 is an important neurodevelopmental transcription factor associated with schizophrenia and Pitt-Hopkins syndrome. In this study, we used genome-wide expression profiling to determine the effects of acute TCF4 knockdown on gene expression in SH-SY5Y neuroblastoma cells. Pathway and enrichment analysis on the differentially expressed genes in TCF4-knockdown cells identified an over-representation of genes involved in TGF-β signaling, epithelial-to-mesenchymal transition (EMT) and apoptosis. Among the most significantly differentially expressed genes were the EMT regulators SNAI2 and DEC1 and the proneural genes NEUROG2 and ASCL1. Altered expression of several mental retardation genes such as UBE3A (AS), ZEB2 (MWS) and MEF2C was also found in TCF4-depleted cells. These data suggest that TCF4 regulates a number of convergent signaling pathways involved in cell differentiation and survival in addition to a subset of clinically important mental retardation genes.

2013-08-20 | GSE48367 | GEO

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