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Retinoic acid rewires the adrenergic core regulatory circuitry of neuroblastoma but can be subverted by enhancer hijacking of MYC or MYCN

ABSTRACT: Retinoic acid rewires the adrenergic core regulatory circuitry of neuroblastoma but can be subverted by enhancer hijacking of MYC or MYCN

PROVIDER: PRJNA648124 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12313400.fastq.gz	Fastqsanger.gz
	SRR12313401.fastq.gz	Fastqsanger.gz
	SRR12313402.fastq.gz	Fastqsanger.gz
	SRR12313403.fastq.gz	Fastqsanger.gz
	SRR12313404.fastq.gz	Fastqsanger.gz

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Retinoic acid rewires the adrenergic core regulatory circuitry of neuroblastoma but can be subverted by enhancer hijacking of MYC or MYCN (ChIP-Seq)

Project description:Retinoic acid rewires the adrenergic core regulatory circuitry of neuroblastoma but can be subverted by enhancer hijacking of MYC or MYCN (ChIP-Seq)

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Retinoic acid rewires the adrenergic core regulatory circuitry of neuroblastoma but can be subverted by enhancer hijacking of MYC or MYCN (RNA-Seq)

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Retinoic acid rewires the adrenergic core regulatory circuitry of neuroblastoma but can be subverted by enhancer hijacking of MYC or MYCN (CUT&RUN-Seq)

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Retinoic acid rewires the adrenergic core regulatory circuitry of neuroblastoma but can be subverted by enhancer hijacking of MYC or MYCN (RNA-Seq)

Project description:Neuroblastoma cell identity depends on a core regulatory circuit (CRC) of transcription factors that incorporate MYCN to drive the oncogenic gene expression program. For neuroblastomas dependent on the adrenergic CRC, treatment with retinoids can inhibit cell growth and induce differentiation in both primary neuroblastomas and cell lines; however, the underlying mechanisms remain unclear. Here we show that when MYCN-amplified neuroblastomas cells are treated with all-trans retinoic acid (ATRA), they undergo modifications of histone H3K27 acetylation and methylation that decommission super-enhancers driving the expression of PHOX2B and GATA3, together with the activation of new super-enhancers that drive high levels of expression of MEIS1, HIC1 and SOX4. These findings indicate that treatment with ATRA can reprogram the enhancer landscape to collapse the adrenergic CRC, which downregulates MYCN expression, while upregulating a new “retino-sympathetic” CRC that causes proliferative arrest and sympathetic differentiation. Thus, we provide mechanisms that account for the beneficial effects of retinoids against high-risk neuroblastoma and explain the rapid downregulation of expression of MYCN despite massive levels of gene amplification.

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Retinoic acid rewires the adrenergic core regulatory circuitry of neuroblastoma but can be subverted by enhancer hijacking of MYC or MYCN (ChIP-Seq)

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Retinoic acid rewires the adrenergic core regulatory circuitry of neuroblastoma but can be subverted by enhancer hijacking of MYC or MYCN (CUT&RUN-Seq)

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Retinoic acid rewires the adrenergic core regulatory circuitry of neuroblastoma but can be subverted by enhancer hijacking of MYC or MYCN

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

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SOX11 regulates SWI/SNF complex components as member of the adrenergic neuroblastoma core regulatory circuitry [4C]

Project description:The pediatric extra-cranial tumor neuroblastoma displays a low mutational burden while recurrent copy number alterations are present in most high-risk cases. We identify SOX11 as a dependency transcription factor in adrenergic neuroblastoma based on recurrent chromosome 2p focal gains and amplifications, specific expression in the normal sympatho-adrenal lineage and adrenergic neuroblastoma, regulation by multiple adrenergic specific (super-)enhancers and strong dependency on high SOX11 expression in adrenergic neuroblastomas. SOX11 regulated direct targets include genes implicated in epigenetic control, cytoskeleton and neurodevelopment. Most notably, SOX11 controls chromatin regulatory complexes, including 10 SWI/SNF core components among which SMARCC1, SMARCA4/BRG1 and ARID1A. Additionally, the histone deacetylase HDAC2, PRC1 complex component CBX2, chromatin-modifying enzyme KDM1A/LSD1 and pioneer factor c-MYB are regulated by SOX11. Finally, SOX11 is identified as a core transcription factor of the core regulatory circuitry (CRC) in adrenergic high-risk neuroblastoma with a potential role as epigenetic master regulator upstream of the CRC.

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SOX11 regulates SWI/SNF complex components as member of the adrenergic neuroblastoma core regulatory circuitry [Cut & Run]

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SOX11 regulates SWI/SNF complex components as member of the adrenergic neuroblastoma core regulatory circuitry [ATAC-Seq]

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