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

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

PROVIDER: PRJNA859872 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR20289053_1.fastq.gz	Fastqsanger.gz
	SRR20289053_2.fastq.gz	Fastqsanger.gz
	SRR20289054_1.fastq.gz	Fastqsanger.gz
	SRR20289054_2.fastq.gz	Fastqsanger.gz
	SRR20289055_1.fastq.gz	Fastqsanger.gz

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

Project description:In this study we identified genes regulated by MYCN, WDR5 and G9a in IMR32 cells

2023-10-19 | GSE208420 | GEO

The cooperation between MYCN and its cofactors WDR5 and G9a on gene transcription regulation [siMYCN]

Project description:MYCN cooperates with WDR5 to activate canonical MYC targets and cooperates with G9a to repress neuronal differentiation genes.

2023-10-19 | GSE208414 | GEO

The cooperation between MYCN and its cofactors WDR5 and G9a on gene transcription regulation [siWDR5]

Project description:MYCN cooperates with WDR5 to activate canonical MYC targets and cooperates with G9a to repress neuronal differentiation genes.

2023-10-19 | GSE208419 | GEO

The cooperation between MYCN and its cofactors WDR5 and G9a on gene transcription regulation [siG9a]

Project description:MYCN cooperates with WDR5 to activate canonical MYC targets and cooperates with G9a to repress neuronal differentiation genes.

2023-10-19 | GSE208417 | GEO

The cooperation between MYCN and its cofactors WDR5 and G9a

Project description:The cooperation between MYCN and its cofactors WDR5 and G9a

| PRJNA859859 | ENA

RNA-sequencing analysis to investigate genes regulated by HAND2 and MYCN in IMR32 cells

Project description:In this study we identified genes regulated by HAND2 or MYCN or both MYCN and HAND2 in IMR32 cells.

2023-03-29 | GSE183609 | GEO

Metabolic dependencies in MYCN-driven neuroblastoma

Project description:Here we sought metabolic alterations specifically associated with amplified MYCN as nodes to indirectly target the MYCN oncogene. Liquid chromatography-mass spectrometry-based proteomics identified 7 proteins consistently correlated with MYCN in proteomes from 49 neuroblastoma biopsies and 13 cell lines. Among these were phosphoglycerate dehydrogenase (PHGDH), the rate-limiting enzyme in de novo serine synthesis. MYCN associated with two regions in the PHGDH promoter, supporting transcriptional PHGDH regulation by MYCN. Pulsed stable isotope-resolved metabolomics utilizing 13C-glucose labeling demonstrated higher de novo serine synthesis in MYCN-amplified cells compared to cells with diploid MYCN. An independence of MYCN-amplified cells from exogenous serine and glycine was demonstrated by serine and glycine starvation, which attenuated nucleotide pools and proliferation only in cells with diploid MYCN but did not diminish these endpoints in MYCN-amplified cells. Proliferation was attenuated in MYCN-amplified cells by CRISPR/Cas9-mediated PHGDH knockout or treatment with PHGDH small molecule inhibitors without affecting cell viability. PHGDH inhibitors administered as single-agent therapy to NMRI-Foxn1nu/nu mice harboring patient-derived MYCN-amplified neuroblastoma xenografts slowed tumor growth. However, combining a PHGDH inhibitor with the standard-of-care chemotherapy drug, cisplatin, revealed antagonism of chemotherapy efficacy in vivo. Emergence of chemotherapy resistance was confirmed in the genetic PHGDH knockout model in vitro. Altogether, PHDGH knockout and inhibition by small molecules consistently slows proliferation, but stops short of killing the cells, which then establish resistance to classical chemotherapy. Although PHGDH inhibition with small molecules has produced encouraging results in other preclinical cancer models, this approach must be considered with caution in patients with neuroblastoma.

2020-12-11 | PXD018300 | 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

Differentiation of IMR32 neuroblastoma is accompanied by a global change in the transcriptome

Project description:The aim of this study is to compare human transcriptomes based on NGS (RNA-seq). The transcriptome of neuroblastoma IMR32 was compared with the transcriptome of neuroblastoma IMR32, which was differentiated for 16 days in the presence of 2.5 mkM BrdU. Methods. Human mRNA profiles of 16-day differentiation of IMR32 neuroblastoma and non-differentiated IMR32 neuroblastoma were obtained by deep three-fold sequencing using Illumina NovaSeq. The mapping is read into the human genome (hg38) using the hisat program. On average, about 89-90% of all data received was unambiguously aligned in each library. The htseq-count utility has counted the number of reads that have been matched against known genes (ncbi - entrezID). The obtained values (cpm - countpermillion) for each gene for each library were combined into one matrix for further analysis. Results: Using an optimized data analysis workflow, we matched about 30 million sequence reads per sample to the human genome (hg38). Filtration, normalization by the method (TMM), variance estimation and differentially expressed genes estimation were performed in the edgeR module. Genes in which the cpm did not exceed 1 in any three libraries were considered low expressing.

2020-12-18 | GSE161759 | 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

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