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

GSE261512 Homo sapiens (human) RNA-seq (gene expression) 20 samples Submitted 2024/11/22 Platform GPL24676
At a glance

RNA-seq (gene expression) · human · 20 samples

What it is
RNA-seq (gene expression)Gene activity measured by sequencing. The summary does not mention single-cell work, so this is most likely bulk: one average per sample, the usual starting point for comparing groups.
Organism
Homo sapiens (human)
Samples
20 samples: 5 conditions, mostly in triplicateGroups are read from the sample names, not from the paper. Check the list below.
Data you can get
A processed table (series matrix) and supplementary files from NCBI; the raw sequencing reads from ENA. Which of these hold counts depends on the study, so check the file list.
Paper
PRMT5 Maintains Tumor Stem Cells to Promote Pediatric High-Grade Glioma TumorigenesisMolecular cancer research : MCR · 2025
Summary (written by the submitters)
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.
Read the full summary ↓
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.
Published in
PRMT5 Maintains Tumor Stem Cells to Promote Pediatric High-Grade Glioma Tumorigenesis
DeSisto J, Balakrishnan I, Knox AJ et al. · Molecular cancer research : MCR 2025 · PMID 39422546 · doi:10.1158/1541-7786.MCR-24-0233
This dataset
Open GSE261512 in finder → Find more human RNA-seq datasets →
Download · which file do I need?

Direct links to NCBI and ENA, no account and no request form. Pick by what you want to do: take the small processed table to look, the supplementary files to re-analyse, or the original raw data to start over.

1 · Just have a look

Processed table

The series matrix: one table of values per sample as the submitters processed it. The smallest download, and it opens in Excel or R. Start here to see what the data look like.

Series matrix ↓
2 · Re-analyse it

Supplementary files

The count tables and other files the authors uploaded. Take only the samples you need, or the whole study as GSE261512_RAW.tar (it can run to tens of gigabytes).

All supplementary files ↗ Whole study · RAW.tar ↓
3 · Start from the raw reads

Raw sequencing reads

The original FASTQ files, straight from the sequencer, held at ENA. Large, and you align them yourself, so only choose this if you need to re-process the study from scratch.

Raw reads on ENA ↗

What the files usually look like: For RNA-seq the counts are usually a table among the supplementary files (look for 'counts', 'expression', 'FPKM' or 'TPM' in the file name). The series matrix of a sequencing study is sometimes nearly empty.

Also filed as BioProject PRJNA1087362 and SRA study SRP495044. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 39422546) ↗
Study design
5 conditions, mostly in triplicate
BT245 cells transduced with PRMT targeting sh… ×3 DIPG4 cells transduced with PRMT targeting sh… ×3 DIPG7 cells transduced with PRMT targeting sh… ×3 DIPG13* cells transduced with PRMT targeting … ×3 GBM1 cells transduced with PRMT targeting shR… ×3 BT245 cells transduced with control shRNA SHC ×1 DIPG4 cells transduced with control shRNA SHC ×1 DIPG7 cells transduced with control shRNA SHC ×1 +2 more

Supports a between-group comparison across 15 samples.

How we read this: 5 replicated groups read from 20 sample titles; they account for 15 of them. These groups are guessed from the sample names, not taken from the paper, so check them against the sample list below before relying on them.

Samples in this study
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