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Differential gene expression analysis of MYCN-amplified neuroblastoma cells after Doxycycline inducible shRNA knockdown of JMJD6 gene expression

ABSTRACT: JMJD6 oncoprotein induces neuroblastoma and exerts its biological effects through modulation of downstream target genes. We identified that JMJD6 knockdown reduces neuroblastoma cell proliferation, so we investigated which downstream signaling pathways were regulated by JMJD6.

ORGANISM(S): Homo sapiens

PROVIDER: GSE112914 | GEO | 2019/06/23

REPOSITORIES: GEO

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Pol2 binding examined by ChIP-seq in inducible JMJD6 knockdown neuroblastoma cells

Project description:JMJD6 is an important oncogene that is upregulated in 17q21-ter gained neuroblastoma.It plays a role in E2F and N-Myc-regulated gene pathways and neuroblastoma tumorigenesis Using ChIP-Seq, We profiled RNA polymerase 2 binding in doxycycline inducible JMJD6 shRNA CHP-134 neuroblastoma cells, treated with either doxycycline or vehicle control. We identified a list of genes with reduced RNA Pol II binding peaks at their gene promoters as a result of the JMJD6 knockdown. GSEA analysis showed that the top four gene sets, with most considerable reduction in RNA Pol II binding peaks at gene promoters, were E2F target genes, G2M checkpoint genes, mitotic spindle genes, and Myc target genes.

2019-06-23 | GSE112919 | 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

Differential gene expression analysis of MYCN-amplified neuroblastoma cells after Doxycycline inducible shRNA knockdown of JMJD6 gene expression

Project description:Differential gene expression analysis of MYCN-amplified neuroblastoma cells after Doxycycline inducible shRNA knockdown of JMJD6 gene expression

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JMJD6 and NMYC binding examined by ChIP-seq in NMYC overexpressing CHP134 human neuroblastoma cells

Project description:JMJD6 (also known as PTDSR) is an important oncogene that is upregulated in 17q21-ter gained neuroblastoma.It plays a role in E2F and N-Myc-regulated gene pathways and neuroblastoma tumorigenesis Using ChIP-Seq, we profiled JMJD6 and NMYC binding in the NMYC overexpressing neuroblastoma cell line. We identified the genomic location of JMJD6 and NMYC binding peaks across the human genome.

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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. 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.

2016-09-08 | E-GEOD-80397 | biostudies-arrayexpress

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The microRNA landscape of MYCN-amplified neuroblastoma

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Metabolic reprogramming of cancer cells by JMJD6-mediated alternative splicing

Project description:Chromosome 17q gain occurs frequently in MYC-driven tumors including high-risk neuroblastoma. However, the biological consequences of this genetic event remain elusive. Here we show that JMJD6, frequently amplified at the chromosome 17q25 locus, is one of the essential genes to neuroblastoma cells that are engaged in pathways of mitochondrial metabolism, RNA processing and protein homeostasis. JMJD6 cooperates with MYC in cellular transformation and promotes cancer cell proliferation and tumor growth. Mechanistically, JMJD6 physically interacts with RNA-processing machinery to regulate the alternative splicing and protein synthesis. Notably, JMJD6 controls the alternative splicing of glutaminase (GLS), kidney-type glutaminase (KGA) and glutaminase C (GAC), a rate-limiting enzyme of glutaminolysis, and, consequently, the central carbon metabolism in neuroblastoma. Our findings indicate that JMJD6 coordinates with MYC in tumorigenesis by regulating cancer-promoting metabolic programs through an alternative pre-mRNA splicing mechanism.

2023-10-31 | GSE185867 | GEO

Super-enhancer Driven Core Regulatory Circuitry in MYCN-amplified Neuroblastoma [array]

Project description:Transcriptional dysregulation plays a major role in the development and progression of human tumors such as pediatric neuroblastoma. Therefore, we sought to elucidate the relationship between genes required for neuroblastoma cell growth and survival and the transcriptional core regulatory circuitry (CRC) that controls the gene expression program. A genome-scale CRISPR-Cas9 screen for oncogenic dependencies revealed that 143 genes are essential for cell survival and growth in neuroblastoma relative to other cancers, including many super-enhancer (SE) regulated transcription factors. Genome-wide occupancy analysis of transcription factor binding demonstrated that at least six of these transcription factors were both dependency genes and components of the CRC in MYCN-amplified neuroblastoma including: HAND2, ISL1, PHOX2B, GATA3, TBX2, and MEIS2. Binding sites for these transcription factors were clustered within a few hundred base pairs in their own enhancers and the enhancers of downstream target genes, which surprisingly included 40% of the independently determined neuroblastoma dependency genes. This profound level of transcriptional control of oncogenesis through self-reinforcing transcriptional circuits led us to test combinatorial pharmacological inhibition of transcriptional initiation and elongation, which synergistically induced tumor cell death, supporting drugging transcription as a means to advance the treatment of high risk neuroblastoma.

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

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2017-12-02 | GSE85430 | GEO

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