GEO series

Connexin 43 drives glioblastoma cancer stem cell phenotypes through a WNK lysine-deficient protein kinase 1-c-MYC signaling axis

GSE272349 Homo sapiens (human) RNA-seq (gene expression) 15 samples Submitted 2025/08/11 Platform GPL24676

At a glance

RNA-seq (gene expression) · human · 15 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)
Topic: GlioblastomaThis series is part of our curated briefing on it.
Samples: 15 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: Connexin 43 drives glioblastoma cancer stem cell phenotypes through a WNK lysine-deficient protein kinase 1-c-MYC signaling axisCell reports · 2025

Summary (written by the submitters)

The coordination of cellular processes such as growth and survival relies on communication between cells through gap junctions. Gap junction intercellular communication is driven by connexin proteins, which also mediate protein-protein interactions and communication with the extracellular space via hemichannels. Despite their essential roles, connexin function in cancer is context dependent, with connexin 43 (Cx43) reported to both promote and suppress tumor growth in glioblastoma, the most common primary malignant brain tumor.

Read the full summary ↓

Here, we detect expression of Cx43 in glioblastoma patient-derived cancer stem cells and demonstrate that Cx43 is essential for their survival and self-renewal. Mechanistically, depletion of Cx43 reduces c-MYC expression through reduced levels of the upstream mediator WNK lysine-deficient protein kinase 1 (WNK1). Depletion of WNK1 phenocopies Cx43 knockdown and reduces MYC expression and tumor growth. Together, these results define a novel signaling axis downstream of Cx43 that promotes tumor growth and cancer stem cell phenotypes in glioblastoma.

Published in

Connexin 43 drives glioblastoma cancer stem cell phenotypes through a WNK lysine-deficient protein kinase 1-c-MYC signaling axis

Mulkearns-Hubert EE, Hajdari N, Hong ES et al. · Cell reports 2025 · PMID 40946315 · doi:10.1016/j.celrep.2025.116303

This dataset

Open GSE272349 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 GSE272349_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 PRJNA1136493 and SRA study SRP520273. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 40946315) ↗

Study design

5 conditions, mostly in triplicate

DI318 cells, non-target shControl, ×3 DI318 cells, Cx43 sh73, ×3 DI318 cells, Cx43 sh77, ×3 DI318 cells, WNK1 sh491, ×3 DI318 cells, WNK1 sh920, ×3

Supports a between-group comparison across 15 samples.

How we read this: 5 replicated groups read from 15 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

GSM8398997 DI318 cells, non-target shControl, biological replicate 1 DI318 cells, non-target…
GSM8398998 DI318 cells, non-target shControl, biological replicate 2 DI318 cells, non-target…
GSM8398999 DI318 cells, non-target shControl, biological replicate 3 DI318 cells, non-target…
GSM8399000 DI318 cells, Cx43 sh73, biological replicate 1 DI318 cells, Cx43 sh73,
GSM8399001 DI318 cells, Cx43 sh73, biological replicate 2 DI318 cells, Cx43 sh73,
GSM8399002 DI318 cells, Cx43 sh73, biological replicate 3 DI318 cells, Cx43 sh73,
GSM8399003 DI318 cells, Cx43 sh77, biological replicate 1 DI318 cells, Cx43 sh77,
GSM8399004 DI318 cells, Cx43 sh77, biological replicate 2 DI318 cells, Cx43 sh77,
GSM8399005 DI318 cells, Cx43 sh77, biological replicate 3 DI318 cells, Cx43 sh77,
GSM8399006 DI318 cells, WNK1 sh491, biological replicate 1 DI318 cells, WNK1 sh491,
GSM8399007 DI318 cells, WNK1 sh491, biological replicate 2 DI318 cells, WNK1 sh491,
GSM8399008 DI318 cells, WNK1 sh491, biological replicate 3 DI318 cells, WNK1 sh491,
GSM8399009 DI318 cells, WNK1 sh920, biological replicate 1 DI318 cells, WNK1 sh920,
GSM8399010 DI318 cells, WNK1 sh920, biological replicate 2 DI318 cells, WNK1 sh920,
GSM8399011 DI318 cells, WNK1 sh920, biological replicate 3 DI318 cells, WNK1 sh920,

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Metadata from NCBI GEO, cached and refreshed periodically — the NCBI page above is authoritative. Downloads link straight to NCBI/ENA; nothing is proxied through BioTransfer.