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The transcriptional repressor SNAI2 impairs neuroblastoma differentiation and inhibits response to retinoic acid therapy

ABSTRACT: The transcriptional repressor SNAI2 impairs neuroblastoma differentiation and inhibits response to retinoic acid therapy

PROVIDER: PRJNA521609 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8554930_1.fastq.gz	Fastqsanger.gz
	SRR8554930_2.fastq.gz	Fastqsanger.gz
	SRR8554921_1.fastq.gz	Fastqsanger.gz
	SRR8554921_2.fastq.gz	Fastqsanger.gz
	SRR8554931_1.fastq.gz	Fastqsanger.gz

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The transcriptional repressor SNAI2 impairs neuroblastoma differentiation and inhibits response to retinoic acid therapy

Project description:Analyses of the effect of CRISPR/CAS9 mediated knock out of the EMT-transcription factor SNAI2 on the mRNA expression profile of human neuroblastoma SH-SY5Y cells to identify genes that are differentially expressed upon loss of SNAI2. Results provide insight into genes that are repressed by SNAI2 in neuroblastoma cells under normal culture conditions, where loss of SNAI2 enhances the expression of genes involved in biological processes such as neuron development and neuron differentiation.

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Snai2 maintains bone marrow niche cells by repressing osteopontin expression

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Super-enhancer-associated core regulatory circuits mediate susceptibility to retinoic acid in neuroblastoma cells [RNA-seq]

Project description:Neuroblastoma is a pediatric tumor that accounts for more than 15% of cancer-related deaths in children. Survival chances for high-risk patients are less than 50%. Retinoic acid treatment is part of the maintenance therapy given to neuroblastoma patients; however, not all tumors respond to retinoic acid-mediated differentiation. Among neuroblastoma tumors, two phenotypically distinct cell types-adrenergic (ADRN) and mesenchymal (MES), have been identified based on their super-enhancer landscape and transcriptional core regulatory circuitries. We hypothesized that distinct super-enhancers in these different tumor cells could mediate differential response to retinoic acid. To this end, we treated four different neuroblastoma cell lines, comprising both ADRN (MYCN amplified and non-amplified) and MES subtypes, with retinoic acid and studied the super-enhancer landscape upon treatment and after removal of retinoic acid. Using H3K27ac ChIP-seq paired with RNA-seq, we compared the super-enhancers in cells that respond to retinoic acid-mediated differentiation versus those that fail to differentiate. We identified unique super-enhancers associated with cells differentiation; however, even among cells that respond to treatment, there was heterogeneity upon removal of retinoic acid, with MYCN amplified cells remaining differentiated whereas MYCN non-amplified cells reverted to a proliferative state. This study identifies regulatory super-enhancers as a plausible mechanism behind the differential response to retinoic acid-mediated differentiation.

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Super-enhancer-associated core regulatory circuits mediate susceptibility to retinoic acid in neuroblastoma cells [ChIP-Seq]

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MYT1 attenuates neuroblastoma cell differentiation by inhibiting retinoic acid signaling pathway

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Neuroblastoma Neuro2A Cell Differentiation induced by retinoic acid-treatment

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Genome-wide maps of SNAI2 binding in undifferentiated and differentiated keratinocytes

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