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Single cell analyses reveals a non-canonical EZH2 activity as main driver of RA resistance in PLZF/RARA leukemia [RNA-seq]

ABSTRACT: Single cell analyses reveals a non-canonical EZH2 activity as main driver of RA resistance in PLZF/RARA leukemia [RNA-seq]

PROVIDER: PRJNA751032 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15305300.fastq.gz	Fastqsanger.gz
	SRR15305301.fastq.gz	Fastqsanger.gz
	SRR15305302.fastq.gz	Fastqsanger.gz
	SRR15305303.fastq.gz	Fastqsanger.gz
	SRR15305304.fastq.gz	Fastqsanger.gz

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Single cell analyses reveals a non-canonical EZH2 activity as main driver of RA resistance in PLZF/RARA leukemia [scRNA-seq]

Project description:Resistance to treatment is due to the heterogeneity of the tumor which contains a subset of cancer cells that escape treatment and are responsible for the relapse. We took advantage of the PLZF/RARA retinoic acid (RA) resistant acute promyelocytic leukemia (APL) model to catch relapse-initiating cell features and their vulnerabilities. By developing an integrative single-cell multi-omics analysis (scRNA-seq and scATAC-seq), we uncovered transcriptional and chromatin heterogeneity of the PLZF/RARA APL blasts. We highlighted a subset of cells insensitive to RA-induced differentiation with a strong DNA repair signature ("Rep" cluster) and exhibiting a fine tuned transcriptional network targeting the histone methyltransferase Ezh2. Combining epigenomic profiling with mouse-derived models for Ezh2 catalytic inhibition or total KO, we revealed an independent methyltransferase Ezh2 activity linked to RA resistance. These findings demonstrate the power of single-cell multi-omics integration to highlight paths to sensitize therapy-resistant leukemia cells

2022-08-22 | GSE181189 | GEO

Single cell analyses reveals a non-canonical EZH2 activity as main driver of RA resistance in PLZF/RARA leukemia [scATAC-seq]

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Single cell analyses reveals a non-canonical EZH2 activity as main driver of RA resistance in PLZF/RARA leukemia [ChIP-seq]

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Single cell analyses reveals a non-canonical EZH2 activity as main driver of RA resistance in PLZF/RARA leukemia [RNA-seq]

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Single cell analyses reveals a non-canonical EZH2 activity as main driver of RA resistance in PLZF/RARA leukemia [RNA-seq]

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Transcription profiling of human U937T:PLZF-RARa Inducible Cells

Project description:The PLZF-RARa fusion oncoprotein is overexpressed in the t(11;17) subtype of acute promyelocytic leukemia. Gene expression microarrays were used to identify genes involved in leukemic transformation. We used microarray to detect gene expression changes induced by the PLZF-RARa fusion oncoprotein in the U937 cell line Experiment Overall Design: The U937T:PLZF-RARa cell line was engineered to express PLZF-RARa upon tetracycline removal. PLZF-RARa was induced for 48hr and RNA was extracted and hybridized to Affymetrix HGU133Plus2.0 Chips

2009-12-05 | E-GEOD-18476 | biostudies-arrayexpress

Gene Expression Data from U937T:PLZF-RARa Inducible Cells

2009-11-30 | GSE18476 | GEO

Transcription profiling of human patients with t(11;17) or t(7;17) translocations and with the RARA-PLZF status known were analysed for changes in expression related to the reciprocal status

Project description:This study supports an active role for PLZF and RARÎ±-PLZF in leukemogenesis, identifies upregulation of CRABPI as a novel mechanism contributing to retinoid resistance and reveals the ability of the reciprocal fusion gene products to mediate distinct; epigenetic effects contributing to the leukemic phenotype. Experiment Overall Design: 5 patients with t(11;17) or t(7;17) translocations and with the RARA-PLZF status known were analysed for changes in expression related to the reciprocal status. This is a rare disease.

2008-06-16 | E-GEOD-8510 | biostudies-arrayexpress

Single cell analyses reveals a non-canonical EZH2 activity as main driver of RA resistance in PLZF/RARA leukemia.

Project description:This SuperSeries is composed of the SubSeries listed below.

2022-08-22 | GSE181190 | GEO

Therapy-induced PML nuclear body re-formation and p53 activation trigger acute promyelocytic leukaemia cure

Project description:The therapy-induced PML/RARA catabolism elicits the loss of APL-initiating cell self-renewal through PML NB reformation and P53 activation. These results explain the curative activity of the RA/arsenic combination, the resistance to RA of PLZF/RARA-driven APLs and they raise the prospect that activation of this PML/P53 checkpoint might have therapeutic values in other malignancies.

2014-01-11 | GSE51723 | GEO

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