GEO series

INSM1 governs a neuronal progenitor state that drives glioblastoma in a human stem cell model

GSE229901 Homo sapiens (human) ChIP-seq / ATAC-seq (genome binding and open chromatin) 15 samples Submitted 2025/07/15 Platform GPL24676

At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · human · 15 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: 15 samples: 13 distinct titles, 1 of them repeatedGroups 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: INSM1 governs a neuronal progenitor state that drives glioblastoma in a human stem cell modelNature communications · 2025

Summary (written by the submitters)

Glioblastoma (GBM) is an aggressivea lethal brain tumorcancer marked by functional plasticity driven by the interplay between tumor cell-intrinsic mutations and -extrinsic heterogeneity, enabling rapid evolutiontheir interplay with developmental programs. To investigate how canonical GBM glioblastoma mutations promote functional plasticity, we have developeded an isogenic human neural stem cell (NSC) model of glioblastoma GBM by sequential addition of TERT promoter, TP53, and PDGFRA point mutations.

Read the full summary ↓

TP53 loss-of-function increasesd TERT TERT expression during serial mutagenesis, but only triple mutant NSCs reliably formed lethal brain tumors in vivo that recapitulate glioblastomaGBM. Tumor cell evolution triggersed stress-related metabolic changes and transitionsed toward a neuronal progenitor network driven by transcription factor INSM1. INSM1 is highly expressed in human glioblastoma GBM tumors and, during cortical development, in intermediate progenitor cells (IPC), which give rise to neurons. Remarkably, INSM1 knockdown in triple mutant NSCs and primary glioblastoma GBM cells disrupted disrupts oncogenic gene expression and function and inhibited inhibits the in vivo tumorigenicity of triple mutant NSCs, highlighting the functional importance of an intermediate progenitor cellIPC-like cell state in glioblastoma GBM pathogenesis.

Published in

INSM1 governs a neuronal progenitor state that drives glioblastoma in a human stem cell model

DeSouza PA, Ishahak M, Qu X et al. · Nature communications 2025 · PMID 41354838 · doi:10.1038/s41467-025-66371-x

This dataset

Open GSE229901 in finder → Find more human RNA-seq 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 GSE229901_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 PRJNA956944 and SRA study SRP433233. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 41354838) ↗

Study design

13 distinct titles, 1 of them repeated

mouse ×3

Supports a case/control comparison: 1 samples read as cases, 4 as controls.

How we read this: Read from 15 sample titles: 13 distinct titles with little repetition. 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

GSM7179939 serial mutants
GSM7179940 WT, rep1 [ATAC]
GSM7179941 WT, rep1 [GEX]
GSM7179942 WT, rep2 [ATAC]
GSM7179943 WT, rep2 [GEX]
GSM7179944 PRO, rep1 [ATAC]
GSM7179945 PRO, rep1 [GEX]
GSM7179946 PRO, rep2 [ATAC]
GSM7179947 PRO, rep2 [GEX]
GSM7179948 mouse-35
GSM7179949 mouse-38
GSM7179950 mouse-42
GSM7179951 INSM1i
GSM7179952 TCF4i
GSM7179953 SOX4i

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