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RNA-seq of IMR-5/75 neuroblastoma cell line upon TBX2 and/or MYCN knockdown

ABSTRACT: RNA-seq of IMR-5/75 neuroblastoma cell line upon TBX2 and/or MYCN knockdown

PROVIDER: PRJEB25334 | ENA |

REPOSITORIES: ENA

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RNA-seq of IMR-5/75 neuroblastoma cell line upon TBX2 and/or MYCN knockdown

Project description:RNA-seq upon TBX2, MYCN or combination of TBX2 and MYCN knockdown in the neuroblastoma cell line IMR-5/75. Cells were transduced with two different shRNAs (shTBX2_2 and shTBX2_4) targeting TBX2 and a non-targeting control (NTC), and selected with puromycin. Cells were treated with doxycycline for shMYCN induction (with DOX or not). Analysis was performed three days upon TBX2 knockdown and two days upon MYCN knockdown, including six biological replicates per condition.

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Project description:ChIP-seq to define bindings sites for TBX2, MYCN, H3K27ac, H3K4me1, H3K4me3 and Input in the cell lines IMR-32, CLB-GA, NGP, IMR-5/75, GI-M-EN, CHP-212, and IMR-5.

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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.

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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

ChIP-seq of neuroblastoma IMR-32, CLB-GA, NGP, IMR-5/75, GI-M-EN, CHP-212, and IMR-5 cell lines to identify TBX2, MYCN, H3K27ac, H3K4me1 and H3K4me3 binding sites

Project description:ChIP-seq of neuroblastoma IMR-32, CLB-GA, NGP, IMR-5/75, GI-M-EN, CHP-212, and IMR-5 cell lines to identify TBX2, MYCN, H3K27ac, H3K4me1 and H3K4me3 binding sites

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RNA-seq of IMR-5/75 neuroblastoma cell line treated with JQ1, THZ1 or combination against untreated controls

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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.

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NB IMR-5/75 medium perturbation

Project description:RNA seq data of human Neuroblastoma IMR-5/75 cell line grown under different medium conditions.

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