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Metabolic licensing of quiescent glioblastoma activation and immune evasion via astrocyte-mitochondria shuttle

GSE294545 Homo sapiens (human) ChIP-seq / ATAC-seq (genome binding and open chromatin) 20 samples Submitted 2025/04/30 Platform GPL24676
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · human · 20 samples

What it is
ChIP-seq / ATAC-seq (genome binding and open chromatin)Where proteins bind the genome, or which regions are open and active.
Organism
Homo sapiens (human)
Topic
GlioblastomaThis series is part of our curated briefing on it.
Samples
20 samples: 10 conditions, mostly in duplicateGroups 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.
Summary (written by the submitters)
The reaction of quiescent tumor cell subpopulations at the invasive margin of glioblastoma (GBM) might be cleared by immune surveillance toward death or expand through immune escape, which can drive therapeutic resistance, tumor dissemination, and recurrence through phenotypic plasticity. However, the process and mechanisms underlying their activation remain largely unclear.
Read the full summary ↓
This study revealed that astrocytes awaken quiescent GBM cells to cycling and immune-evasive phenotypes. Astrocytic mitochondria are indispensable in regulating the phenotypic changes. Specifically, the SHMT2 enzyme in astrocytic mitochondria catalyzes one-carbon metabolic products, which significantly promote synthetic metabolic activation and reactivation of quiescent GBM cells to immune evasion through intercellular mitochondrial transfer. Tumor cells that acquire astrocytic mitochondria enhanced one-carbon metabolism drives global hyperactive anabolic metabolism through YTHDC1-mediated transcriptional pause release of ribosomal and focal adhesion signaling genes, supporting rapid proliferation and conferring a potent immune-evasive phenotype. Therapeutically, pharmacologic or genetic inhibiting the astrocytic SHMT2 or blocking mitochondrial transfer markedly suppressed quiescent GBM cell activation and tumor progression. These findings elucidate a novel mechanism by which astrocytes in the tumor microenvironment drive GBM malignancy through metabolic symbiosis.
This dataset
Open GSE294545 in finder → Find more human ChIP / ATAC / CUT&Tag datasets → Glioblastoma landscape →
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 GSE294545_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: Look for peak files (.bed, .narrowPeak) and signal tracks (.bigWig) among the supplementary files; the raw reads are on ENA.

Also filed as BioProject PRJNA1250475 and SRA study SRP578418. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗
Study design
10 conditions, mostly in duplicate
U87-CTD-RNAPII_S2P ×2 U87+AstWT-CTD-RNAPII_S2P ×2 U87+Astshmt2 KO-CTD-RNAPII_S2P ×2 U87-CTD-RNAPII_S5P ×2 U87+AstWT-CTD-RNAPII_S5P ×2 U87+Astshmt2 KO-CTD-RNAPII_S5P ×2 U87WT+Ast-CTD-RNAPII_S5P ×2 U87YTHDC1 KD+Ast-CTD-RNAPII_S5P ×2 +2 more

Supports a between-group comparison across 20 samples.

How we read this: 10 replicated groups read from 20 sample titles; they account for 20 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
More Glioblastoma datasets

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