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PRMT5 promotes growth of pediatric high grade glioma [ChIP-seq]

ABSTRACT: PRMT5 promotes growth of pediatric high grade glioma [ChIP-seq]

PROVIDER: PRJNA1087361 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28335334_1.fastq.gz	Fastqsanger.gz
	SRR28335334_2.fastq.gz	Fastqsanger.gz
	SRR28335335_1.fastq.gz	Fastqsanger.gz
	SRR28335335_2.fastq.gz	Fastqsanger.gz
	SRR28335336_1.fastq.gz	Fastqsanger.gz

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PRMT5 promotes growth of pediatric high grade glioma.

Project description:PRMT5 promotes growth of pediatric high grade glioma.

| PRJNA1087354 | ENA

PRMT5 promotes growth of pediatric high grade glioma [ChIP-seq]

Project description:Background. Pediatric high-grade gliomas (PHGG) are aggressive, undifferentiated CNS tumors with poor outcomes, for which no standard-of-care drug therapy currently exists. Through a knockdown screen for epigenetic regulators, we identified PRMT5 as essential for PHGG cell growth. We hypothesized that, similar to its effect in normal cells, PRMT5 promotes self-renewal of stem-like PHGG tumor initiating cells (TICs) essential for tumor growth. Methods. We conducted in vitro analyses, including limiting dilution studies of self-renewal, to determine the phenotypic effects of PRMT5 KD. We performed ChIP-Seq to identify PRMT5-mediated epigenetic changes and gene set enrichment analysis to identify pathways that PRMT5 regulates. Using an orthotopic xenograft model of PHGG, we tracked survival and histological characteristics resulting from PRMT5 KD or administration of a PRMT5 inhibitor ± radiation therapy (RT). Results. In vitro, PRMT5 KD slowed cell cycle progression, tumor growth and self-renewal. PRMT5 KD reduced H3K4me3 occupancy at genes associated with self-renewal, tumor formation and growth. In vivo, PRMT5 KD increased survival and reduced tumor aggressiveness; however, pharmacological inhibition of PRMT5 with or without RT did not improve survival. Conclusion. PRMT5 KD epigenetically reduced TIC self-renewal, leading to increased survival in preclinical models. Pharmacological inhibition of PRMT5 enzymatic activity may have failed in vivo due to insufficient reduction of PRMT5 activity by chemical inhibition, or this failure may suggest that non-enzymatic activities of PRMT5 are more relevant.

2024-11-22 | GSE261513 | GEO

PRMT5 promotes growth of pediatric high grade glioma [bulk RNA-seq]

Project description:PRMT5 promotes growth of pediatric high grade glioma [bulk RNA-seq]

| PRJNA1087362 | ENA

PRMT5 promotes growth of pediatric high grade glioma [bulk RNA-seq]

2024-11-22 | GSE261512 | GEO

Tumor and immune cell types interact to produce heterogeneous phenotypes of pediatric high grade glioma [bulkRNA-seq]

Project description:Bulk RNA-Seq of pediatric high-grade glioma patient samples

2023-11-03 | GSE231858 | GEO

PRMT5 promotes growth of pediatric high grade glioma.

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

2024-11-22 | GSE261514 | GEO

Tumor and immune cell types interact to produce heterogeneous phenotypes of pediatric high grade glioma [scRNA-seq]

Project description:Single-cell RNA-Seq was conducted on 19 pediatric high-grade glioma patient samples to study tumor heterogeneity and tumor/immune cell interaction.

2023-11-03 | GSE231859 | GEO

Effect of disulfiram treatment on pediatric high grade glioma

Project description:Effect of disulfiram treatment on pediatric high grade glioma

| PRJNA577636 | ENA

Single-cell ATAC-Seq of pediatric high-grade glioma

Project description:Single-cell ATAC-Seq of pediatric high-grade glioma

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Gene expression (RNA-Seq) in pediatric high-grade glioma cell lines treated with selinexor and vehicle

Project description:Cultured pediatric high-grade glioma cell lines (SU-DIPG-IV, HSJD-DIPG-007, HSJD-GBM-001,BT 245 (RRID:CVCL_IP13)) were treated with selinexor (Karyopharm Therapeutics) at 5xIC50 for 16 hours or vehicle (0.1% DMSO) followed by bulk RNA-Seq

2020-01-06 | GSE137702 | GEO

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