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C-MYC drives neuroblastoma tumorigenesis and retinoic acid resistance in zebrafish

ABSTRACT: c-MYC drives neuroblastoma tumorigenesis and retinoic acid resistance in zebrafish

PROVIDER: PRJNA388873 | ENA |

REPOSITORIES: ENA

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c-MYC drives neuroblastoma tumorigenesis and retinoic acid resistance in zebrafish [RNA-Seq]

Project description:Neuroblastoma is an often intractable tumor that accounts for 15% of childhood cancer deaths. In addition to MYCN amplification in 20% of tumors, 11% express high levels of c-MYC (MYC) protein. To study this newly defined subgroup, we have created a novel transgenic zebrafish model in which overexpression of MYC in the peripheral sympathetic nervous system drives early-onset neuroblastoma.

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c-MYC drives neuroblastoma tumorigenesis and retinoic acid resistance in zebrafish [ATAC-Seq]

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c-MYC drives neuroblastoma tumorigenesis and retinoic acid resistance in zebrafish

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

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The transcriptional co-repressor Runx1t1 is essential for MYCN-driven neuroblastoma tumorigenesis

Project description:Changes in epigenetic regulation are believed to be a major contributing factor to neuroblastoma development. Using a large-scale in vivo mutagenesis screen in Th-MYCN transgenic mice, we identified a single point mutation in the transcriptional corepressor Runx1t1, that can block N-myc-driven neuroblastoma tumorigenesis. The loss of function mutation disrupts a highly conserved zinc finger domain (NHR4) within Runx1t1. Crossing an independent Runx1t1 knockout model with Th-MYCN mice, demonstrated that Runx1t1 haploinsufficiency is enough to prevent neuroblastoma development and reverse ganglia hyperplasia. Silencing RUNX1T1 in human neuroblastoma cells resulted in decreased colony formation in vitro, and significant inhibition of tumor growth in vivo. Our results show that RUNX1T1 forms part of a transcriptional LSD1-CoREST3-HDAC repressive complex that regulates the epigenomic landscape and chromatin accessibility, to control neuron-specific pathway genes and maintain an undifferentiated state. Runx1t1 thus represents an entirely novel and highly promising target not previously described in neuroblastoma.

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The transcriptional co-repressor Runx1t1 is essential for N-Myc-driven neuroblastoma tumorigenesis [RNA-Seq 2]

Project description:Changes in epigenetic regulation are believed to be a major contributing factor to neuroblastoma development. Using a large-scale in vivo mutagenesis screen in Th-MYCN transgenic mice, we identified a single point mutation in the transcriptional corepressor Runx1t1, that can block N-Myc-driven neuroblastoma tumorigenesis. The loss of function mutation disrupts a highly conserved zinc finger domain (NHR4) within Runx1t1. Crossing an independent Runx1t1 knockout model with Th-MYCN mice, demonstrated that Runx1t1 haploinsufficiency is enough to prevent neuroblastoma development and reverse ganglia hyperplasia. Silencing RUNX1T1 in human neuroblastoma cells resulted in decreased colony formation in vitro, and significant inhibition of tumor growth in vivo. Our results show that RUNX1T1 forms part of a transcriptional LSD1-CoREST3-HDAC repressive complex that regulates the epigenomic landscape and chromatin accessibility, to control neuron-specific pathway genes and maintain an undifferentiated state. Runx1t1 thus represents an entirely novel and highly promising target not previously described in neuroblastoma.

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The transcriptional co-repressor Runx1t1 is essential for N-Myc-driven neuroblastoma tumorigenesis [RNA-Seq 1]

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The transcriptional co-repressor Runx1t1 is essential for N-Myc-driven neuroblastoma tumorigenesis

Project description:The transcriptional co-repressor Runx1t1 is essential for N-Myc-driven neuroblastoma tumorigenesis

| PRJNA958148 | ENA

RNF4 sustains Myc-driven tumorigenesis by facilitating DNA replication

Project description:RNF4 sustains Myc-driven tumorigenesis by facilitating DNA replication

2022-08-16 | MSV000090142 | MassIVE

The histone H3 lysine 4 presenter WDR5 induces N-Myc target gene transcription and promotes neuroblastoma [ChIP-Seq]

Project description:WDR5 is an important co-factor for N-Myc-regulated transcriptional activation and tumorigenesis Using ChIP-Seq, We profiled key epigenetic marks H3K4 trimethylation in BE(2)-C neuroblastoma cells transfected with control siRNA or WDR5 siRNA-1 at N-Myc target gene promoters The results showed knockdown WDR5 significantly reduced H3K4me3 at 93.2% of N-Myc binding promoters, but only at 53.5% of N-Myc non-binding promoters. Identification of Histone H3K4 trimethylation and N-Myc binding sites in BE(2)-C cells transfected with control siRNA or WDR5 siRNA-1.

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