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E-MEXP-149

ABSTRACT: Transcription profiling of blasts from three APL patients expressing PML/RAR before and after treatment with 1 uM retinoic acid (RA) in vitro for four hours

PROVIDER: E-MEXP-149 | ExpressionAtlas | 2025-01-22

REPOSITORIES: ExpressionAtlas

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			Action	DRS
	E-MEXP-149-analysis-methods.tsv	Tabular
	E-MEXP-149-atlasExperimentSummary.Rdata	Rdata
	E-MEXP-149-configuration.xml	Xml
	E-MEXP-149-percentile-ranks.tsv	Tabular
	E-MEXP-149.condensed-sdrf.tsv	Tabular

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Transcription profiling of blasts from three APL patients expressing PML/RAR before and after treatment with 1 uM retinoic acid (RA) in vitro for four hours

Project description:Gene expression profiles in blasts from three APL patients expressing PML/RAR were assessed before and after treatment with 1 uM retinoic acid (RA) in vitro for four hours. We then studied a U937 clone conditionally expressing PML/RAR (U937-PR), (Grignani et al. 1993) (Alcalay et al. 2003), and compared the gene expression profile prior to and after 4 hours of treatment with 1 uM RA, to that obtained from a cell line bearing an empty vector (U937-MT). For each sample, biotinylated cRNA targets were synthesized starting from 5ug of total RNA, and hybridized to the complete set of HG-U133 Affymetrix oligonucleotide chips, which explores the expression of approximately 45,000 human transcripts. Results were analyzed using MASv5 and further elaborated with the GenePicker software. GeneChip probe sets regulated by RA in each sample were clustered into non-redundant regulated genes according to UniGene release Hs.166.

2004-12-31 | E-MEXP-149 | biostudies-arrayexpress

Super-enhancer-associated core regulatory circuits mediate susceptibility to retinoic acid in neuroblastoma cells [ChIP-Seq]

Project description:Neuroblastoma is a pediatric tumor that accounts for more than 15% of cancer-related deaths in children. Survival chances for high-risk patients are less than 50%. Retinoic acid treatment is part of the maintenance therapy given to neuroblastoma patients; however, not all tumors respond to retinoic acid-mediated differentiation. Among neuroblastoma tumors, two phenotypically distinct cell types-adrenergic (ADRN) and mesenchymal (MES), have been identified based on their super-enhancer landscape and transcriptional core regulatory circuitries. We hypothesized that distinct super-enhancers in these different tumor cells could mediate differential response to retinoic acid. To this end, we treated four different neuroblastoma cell lines, comprising both ADRN (MYCN amplified and non-amplified) and MES subtypes, with retinoic acid and studied the super-enhancer landscape upon treatment and after removal of retinoic acid. Using H3K27ac ChIP-seq paired with RNA-seq, we compared the super-enhancers in cells that respond to retinoic acid-mediated differentiation versus those that fail to differentiate. We identified unique super-enhancers associated with cells differentiation; however, even among cells that respond to treatment, there was heterogeneity upon removal of retinoic acid, with MYCN amplified cells remaining differentiated whereas MYCN non-amplified cells reverted to a proliferative state. This study identifies regulatory super-enhancers as a plausible mechanism behind the differential response to retinoic acid-mediated differentiation.

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Super-enhancer-associated core regulatory circuits mediate susceptibility to retinoic acid in neuroblastoma cells [RNA-seq]

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Project description:This study compared the gene expression change of glioblastoma stem-like cells before and after retinoic acid treatment

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RNA-Seq of SH-SY5Y cells after DLG2 overexpression

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