Genome wide N-MYC binding in human inv(16) AML cells
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA947529 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR23939319_1.fastq.gz | Fastqsanger.gz | |||
| SRR23939319_2.fastq.gz | Fastqsanger.gz | |||
| SRR23939320_1.fastq.gz | Fastqsanger.gz | |||
| SRR23939320_2.fastq.gz | Fastqsanger.gz | |||
| SRR23939321_1.fastq.gz | Fastqsanger.gz |
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Project description:Cancer cells maintain a sensitive balance between growth-promoting oncogenes and apoptosis inhibitors. We show that WT RUNX1 is required for survival of t(8;21)-Kasumi-1 and inv(16)-ME-1 AML cell lines. The malignant AML phenotype is sustained by a delicate AML1-ETO/RUNX1 balance that involves competition for common DNA binding sites regulating a subset of AML1-ETO/RUNX1 targets. Genome expression was profiled after performing knockdown of RUNX1 and AML1-ETO in Kasumi-1 cells using specific siRNA-oligo nucleotides, and analyzed using Affymetrix Gene 1.0 ST arrays.
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