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STING Mediates Increased Self-Renewal and Lineage Skewing in DNMT3A-Mutated Hematopoietic Stem/Progenitor Cells

GSE278208 Mus musculus (mouse) RNA-seq (gene expression) 40 samples Submitted 2024/12/19 Platform GPL24247
At a glance

RNA-seq (gene expression) · mouse · 40 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
Mus musculus (mouse)
Samples
40 samples: 12 conditions, mostly with about 4 replicates eachGroups 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
STING mediates increased self-renewal and lineage skewing in DNMT3A-mutated hematopoietic stem/progenitor cellsLeukemia · 2025
Summary (written by the submitters)
Somatic mutations in DNA methyltransferase 3A (DNMT3A) are frequently observed in patients with hematological malignancies. Hematopoietic stem/progenitor cells (HSPCs) with mutated DNMT3A demonstrate increased self-renewal activity and skewed lineage differentiation. However, the molecular mechanisms underlying these changes remain largely unexplored.
Read the full summary ↓
In this study, we show that Dnmt3a loss leads to the upregulation of endogenous retroviruses (ERVs) in HSPCs, subsequently activating the cGAS-STING pathway and triggering inflammatory responses in these cells. Both genetic and pharmacological inhibition of STING effectively corrects the increased self-renewal activity and differentiation skewing induced by Dnmt3a deficiency in mice. Notably, targeting STING showed inhibited acute myeloid leukemia (AML) development in a Dnmt3a-KO; Flt3-ITD AML model, comparable to AC220, an FDA-approved FLT3-ITD inhibitor. A patient-derived xenograft (PDX) model further demonstrated that targeting STING effectively alleviates the leukemic burden of DNMT3A-mutant AML. Collectively, our findings highlight a critical role for STING in hematopoietic disorders induced by DNMT3A mutations and propose STING as a potential therapeutic target for preventing the progression of DNMT3A mutation-associated leukemia.
Published in
STING mediates increased self-renewal and lineage skewing in DNMT3A-mutated hematopoietic stem/progenitor cells
Huang J, Xie J, Wang Y et al. · Leukemia 2025 · PMID 39987368 · doi:10.1038/s41375-025-02542-5
This dataset
Open GSE278208 in finder → Find more mouse 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 GSE278208_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 PRJNA1166095 and SRA study SRP535245. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 39987368) ↗
Study design
12 conditions, mostly with about 4 replicates each
CMPs and GMPs, DNMT3A knockout, ×4 CMPs and GMPs, Wild Type, ×4 long-term HSCs, DNMT3A knockout, ×4 long-term HSCs, Wild Type, ×4 MEPs, DNMT3A knockout, ×4 short-term HSCs, DNMT3A knockout, ×4 short-term HSCs, Wild Type, ×4 c-kit+ bone marrow cells, DNMT3A/STING double… ×3 +4 more

Supports a case/control comparison: 23 samples read as cases, 17 as controls.

How we read this: 12 replicated groups read from 40 sample titles; they account for 40 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
Datasets on a similar topic

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