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MYT1 attenuates neuroblastoma cell differentiation by inhibiting retinoic acid signaling pathway

ABSTRACT: MYT1 attenuates neuroblastoma cell differentiation by inhibiting retinoic acid signaling pathway

PROVIDER: PRJNA526212 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8699492_1.fastq.gz	Fastqsanger.gz
	SRR8699492_2.fastq.gz	Fastqsanger.gz
	SRR8699493_1.fastq.gz	Fastqsanger.gz
	SRR8699493_2.fastq.gz	Fastqsanger.gz
	SRR8699494_1.fastq.gz	Fastqsanger.gz

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MYT1 attenuates neuroblastoma cell differentiation by inhibiting retinoic acid signaling pathway

Project description:This study first reveals that MYT1 is a potential oncogene in neuroblastoma, which is significantly correlated with poor prognosis and represses cellular differentiation via interrupting retinoic acid signaling pathway.

2019-12-01 | GSE128054 | GEO

Identification of Myt1 as a subunit of the neural cell type-specific LSD1 complex

Project description:Regulation of spatiotemporal gene expression in higher eukaryotic cells is critical for the precise and orderly development of undifferentiated progenitors into committed cell types of the adult. Recently, dynamic epigenomic regulation, including chromatin remodeling and histone modifications by transcriptional coregulator complexes, has been shown to be involved in transcriptional regulation. Precisely how these coregulator complexes exert their cell-type and developing stage-specific activity is largely unknown. In this study, we aimed to isolate the histone demethylase LSD1 complex from neural cells by biochemical purification. In so doing, we identified MyT1 as a novel LSD1 complex component. MyT1 is a neural cell-specific zinc finger factor and it forms a stable multiprotein complex with LSD1 through direct interaction. Target gene analysis using microarray and ChIP assays revealed several genes, including PTEN, that were directly regulated by the LSD1-MyT1 complex. Knockdown of either LSD1 or MyT1 derepressed the expression of endogenous target genes and inhibited cell proliferation of a neuroblastoma cell line, Neuro2a. We propose that formation of tissue-specific combinations of coregulator complexes is a critical mechanism for tissue-specific transcriptional regulation. Neuro2a cells were treated with either siControl, siLSD1 or siMyT1 for 48 h (n=3)

2014-05-20 | E-GEOD-49685 | biostudies-arrayexpress

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

2022-07-28 | GSE202239 | GEO

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

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ChIP-Seq MyT1-HA in NS5

Project description:Here we performed a ChIP-seq experiment on a sample of adherent cultures of mouse neural stem cells (NS5 cell line) expressing an inducible HA-tagged version of the proneural factor MyT1 (MyT1-HA, under TetON control) after activation by doxycycline hyclate (DOX). This resulted in the generation of a genome-wide map of MyT1-HA binding to chromatin.

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Identification of Myt1 as a subunit of the neural cell type-specific LSD1 complex

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Neuroblastoma Neuro2A Cell Differentiation induced by retinoic acid-treatment

Project description:To investigate a role of mKIAA genes in early stage of neurite outgrowth, in vitro time course experiment was performed using the mouse neuroblastoma Neuro2A cells and all-trans-retinoic acid. Six time points of 8 biological replicates were performed.These data were normalized by median intensities and subtracted background intensities. NOTE: Outlier involved several data were not deposited. Keywords: time-course

2005-04-28 | GSE2570 | GEO

Cdk8 attenuates lipogenesis by inhibiting SREBP-dependent transcription in Drosophila

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Paraspeckle protein NONO attenuates vascular calcification by inhibiting BMP2 transcription

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Microarray of MyT1 Gain-of-Function in NS5

Project description:Here we performed a microarray experiment on samples of adherent cultures of mouse neural stem cells (NS5 cell line) expressing an inducible version of the transcription factor MyT1 (MyT1-V5 TetON) under normal growth conditions and after 4 hours of treatment by doxycyline. This resulted in the generation of a genome-wide mRNA expression pattern and quantification for these cells in the two conditions.

2016-09-09 | E-MTAB-4335 | biostudies-arrayexpress

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