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RNA-sequencing analysis to identify genes regulated by MYCN in neuroblastoma cell line KCNR.

ABSTRACT: RNA-sequencing analysis to identify genes regulated by MYCN in neuroblastoma cell line KCNR.

PROVIDER: PRJNA859871 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR20289219_1.fastq.gz	Fastqsanger.gz
	SRR20289219_2.fastq.gz	Fastqsanger.gz
	SRR20289220_1.fastq.gz	Fastqsanger.gz
	SRR20289220_2.fastq.gz	Fastqsanger.gz
	SRR20289221_1.fastq.gz	Fastqsanger.gz

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RNA-sequencing analysis to identify genes regulated by MYCN in neuroblastoma cell line SHEP by MYCN overexpression

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RNA-sequencing analysis to identify genes regulated by MYCN, WDR5 and G9a in neuroblastoma cell line IMR32

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Global transcriptome analysis in the MYCN-amplified neuroblastoma cell line IMR5-75 upon inducible MYCN-knockdown

Project description:Inducible MYCN-knockdown, followed by RNA-seq analysis in the MYCN-amplified neuroblastoma cell line IMR5-75, reveals profound time-dependent transcriptome changes.

2016-09-08 | GSE80397 | GEO

Global transcriptome analysis in the MYCN-amplified neuroblastoma cell line IMR5-75 upon inducible MYCN-knockdown

Project description:Inducible MYCN-knockdown, followed by RNA-seq analysis in the MYCN-amplified neuroblastoma cell line IMR5-75, reveals profound time-dependent transcriptome changes. For modulation of MYCN levels, stable neuroblastoma cell models were used where MYCN can be downregulated via vector-based hairpin RNA induction upon addition of 1Âµg/ml tetracycline (IMR5-75-shMYCN. From cells treated either with tetracycline or solvent (ethanol), RNA was isolated at time points 6 hours, 12 hours and 24 hours. Experiments were done in duplicates. RNA was sequenced.

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Genome-wide mapping of MYCN binding in neuroblastoma cells

Project description:To identify the MYCN transcription factor binding sites across the genome, we performed chromatin immunoprecipitation followed by sequencing (ChIP-seq) using anti-MYCN and anti-IgG antibodies on a MYCN-amplified NB cell line, SK-N-BE(2)-C. Identification of MYCN binding in neuroblastoma cells.

2016-05-16 | E-GEOD-72640 | biostudies-arrayexpress

RNA-sequencing analysis to identify genes regulated by MYCN in neuroblastoma cell line SHEP by MYCN overexpression

Project description:In this study we identified genes regulated by MYCN in SHEP cells

2023-10-19 | GSE208422 | GEO

RNA-sequencing analysis to identify genes regulated by MYCN in neuroblastoma cell line KCNR.

Project description:In this study we identified genes regulated by MYCN in KCNR cells

2023-10-19 | GSE208421 | GEO

The Super Elongation Complex Drives Transcriptional Addiction in MYCN-amplified Neuroblastoma

Project description:MYCN amplification in neuroblastoma leads to aberrant expression of MYCN oncoprotein, which binds active genes promoting transcriptional amplification. Yet how MYCN coordinates transcription elongation to meet productive transcriptional amplification and which elongation machinery represents MYCN-driven vulnerability remain to be identified. We conducted a targeted screen of transcription elongation factors and identified the super elongation complex (SEC) as a unique vulnerability in MYCN-amplified neuroblastomas. MYCN directly binds EAF1 and recruits SEC to enhance processive transcription elongation. Depletion of EAF1 or AFF1/AFF4, another core subunit of SEC, leads to a global reduction in transcription elongation and elicits selective apoptosis of MYCN-amplified neuroblastoma cells. A combination screen reveals SEC inhibition synergistically potentiates the therapeutic efficacies of FDA-approved BCL2 antagonist ABT-199, in part due to suppression of MCL1 expression, both in MYCN-amplified neuroblastoma cells and in patient-derived xenografts. These findings identify disruption of the MYCN-SEC regulatory axis as a promising therapeutic strategy in neuroblastoma.

2023-05-10 | PXD039332 | Pride

Dickkopf-1 is down-regulated by MYCN and inhibits neuroblastoma cell proliferation

Project description:Neuroblastomas are tumors of the developing peripheral sympathetic nervous system, which originates from the neural crest. Twenty percent of neuroblastomas show amplification of the MYCN oncogene, which correlates with poor prognosis. The MYCN transcription factor can activate and repress gene expression. To broaden our insight in the spectrum of genes down-regulated by MYCN, we generated gene expression profiles of the neuroblastoma cell lines SHEP-21N and SKNAS-NmycER, in which MYCN activity can be regulated. In this study, we show that MYCN suppresses the expression of Dickkopf-1 (DKK1) in both cell lines. DKK1 is a potent inhibitor of the wnt/beta-catenin signalling cascade, which is known to function in neural crest cell migration. We generated a DKK1 inducible cell line, IMR32-DKK1, which showed impaired proliferation upon DKK1 expression. Surprisingly, DKK1 expression did not inhibit the canonical wnt/beta-catenin signalling, suggesting a role of DKK1 in an alternative route of the wnt pathway. Gene expression profiling of two IMR32-DKK1 clones showed that only a few genes, amongst which SYNPO2, were up-regulated by DKK1. SYNPO2 encodes an actin-binding protein and was previously found to inhibit proliferation and invasiveness of prostate cancer cells. These results suggest that MYCN might stimulate cell proliferation by inhibiting the expression of DKK1. DKK1 might exert part of its growth suppressive effect by induction of SYNPO2 expression. Keywords: DKK1, MYCN, neuroblastoma, Dickkopf

2007-08-24 | GSE8066 | GEO

Targeting EZH2 in MYCN-amplified Neuroblastoma [ChIP-seq]

Project description:Purpose: Identify new targets in MYCN-amplified Neuroblastoma Methods: ChIP-Seq experiments were performed on Kelly and LAN-1 neuroblastoma cells by using the following antibodies: anti-EZH2 (Cell Signaling 5246S); anti-H3K27me3 (Millipore 07-449); anti-H3K4me3 (Abcam ab8580). We evaluated the global EZH2 PRC2-dependence by identifiying direct genome-wide target genes for EZH2, H3K27me3 and H3K4me3. Results: We found that EZH2 serves a PRC2-dependent function in neuroblastoma, repressing neuronal differentiation. Moreover, EZH2-regulated genes were strongly repressed in MYCN-amplified and high-risk primary tumors. Conclusion: Our study supports testing EZH2 inhibitors in patients with MYCN-amplified neuroblastoma.

2017-12-02 | GSE85430 | GEO

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