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RNA-seq analysis in RPMI-8402 cells after knockout of MYC and MYCN

ABSTRACT: RNA-seq analysis was performed in a RPMI-8402 T-ALL cell stably expressing Cas9 aafter knockout of both MYC and MYCN

ORGANISM(S): Homo sapiens

PROVIDER: GSE231962 | GEO | 2023/08/16

REPOSITORIES: GEO

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RNA-seq analysis in RPMI-8402 cells after knockout of MYCN

Project description:RNA-seq analysis was performed in a RPMI-8402 T-ALL cell stably expressing Cas9 after knockout of MYCN

2023-08-16 | GSE231959 | GEO

RNA-seq analysis in RPMI-8402 cells after knockout of MYC

Project description:RNA-seq analysis was performed in a RPMI-8402 T-ALL cell stably expressing Cas9 after knockout of MYC

2023-08-16 | GSE231960 | GEO

H3K27ac Hi-ChIP analysis in Jurkat and RPMI-8402 T-ALL cells

Project description:H3K27ac Hi-ChIP analysis was performed in Jurkat and RPMI-8402 stably expressing dCAR9-KRAB after treatment with DMSO (Control) or Doxycycline to induce sgRNA expression to block MYCN enhnacer region

2023-08-16 | GSE231957 | GEO

ATAC-seq analysis for Jurkat nd RPMI-8402 T-ALL cells

Project description:ATAC-seq analysis was performed in Jurkat and RPMI-8402 to analyze chromatin accessibility at steady state

2023-08-16 | GSE231955 | GEO

Genome wide analysis of binding regions for MYC, MYCN and various histone modifications using Cut&Run

Project description:Cut&Run analysis was performed in RPMI-8402 cells to analyze binding regions of MYC, MYCN and various histone modifications in normal culture conditions

2023-08-16 | GSE231963 | GEO

TAL1 complex in human T-cell acute lymphoblastic leukemia (RPMI-8402)

2012-07-09 | GSE39179 | GEO

TAL1 complex in human T-cell acute lymphoblastic leukemia (RPMI-8402)

Project description:The oncogenic transcription factor TAL1/SCL is aberrantly overexpressed in over 40% of cases of T-cell acute lymphoblastic leukemia (T-ALL), emphasizing the importance of the TAL1-regulated transcriptional program in the molecular pathogenesis of T-ALL. Here we identify regions occupied by TAL1 and its regulatory partners HEB, E2A, and GATA3 in a T-ALL cell line (RPMI-8402). Human T-ALL cells were cross-linked with formaldehyde for 20 min. DNA was enriched by chromatin immunoprecipitation (ChIP) and analyzed by Solexa sequencing. A sample of whole cell extract (WCE) was sequenced and used as the background to determine enrichment. ChIP was performed using an antibody against total TAL1 (Santa Cruz SC-12984), TCF12/HEB (Santa Cruz SC-357),TCF3/E2A (Santa Cruz SC-349X), and GATA3 (Santa Cruz SC-22206).

2012-07-09 | E-GEOD-39179 | biostudies-arrayexpress

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

Expression analysis of T-ALL cell lines TALL-1, RPMI-8402, SUPT11 and P12-ICHIKAWA after treatment with NVS-ZP7-3

Project description:Expression analysis of T-ALL cell lines TALL-1, RPMI-8402, SUPT11 and P12-ICHIKAWA after treatment with NVS-ZP7-3

| PRJNA475768 | ENA

3prime RNA-seq of murine SCLC cell line modified with CRISPR-activation of Myc, Mycl or Mycn

Project description:In cells derived from a genetically engineered Rb1 and Trp53 loss mouse model of SCLC (RP) expression of one of the three MYC family members induced from the endogenous locus using CRISPR activation. Cells were first stably transfected with the lenti-MS2-p65-HSF1 activator plasmid. Respective sgRNAs targeting either Myc, Mycl or MYCN were then cloned into the lentiSAMv2 system and transfected separately into the MS2-p65-HSF1 cells using lentiviral delivery.

2019-07-09 | E-MTAB-7411 | biostudies-arrayexpress

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