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Targeting the ADAR1 p150 isoform triggers tumor growth inhibition and antitumor immunity to overcome immunotherapy resistance

GSE316054 Mus musculus (mouse) RNA-seq (gene expression) 52 samples Submitted 2026/04/12 Platform GPL24676Platform GPL24247
At a glance

RNA-seq (gene expression) · mouse · 52 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
52 samples: 26 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.
Paper
Targeting ADAR1 p150 triggers tumor inhibition and antitumor immunity to overcome immunotherapy resistanceiScience · 2026
Summary (written by the submitters)
Cancer immunotherapy efficacy is often limited by primary and acquired resistance. The RNA- editing enzyme ADAR1 has emerged as a key regulator of tumor immune evasion, yet therapeutic targeting is challenged by the essential physiological roles of its constitutively expressed p110 isoform. Here, we identify the interferon-inducible p150 isoform and its Zα domain as a critical therapeutic vulnerability.
Read the full summary ↓
We demonstrate that ADAR1 p150 is frequently overexpressed in human cancers and correlates with an immunosuppressive tumor microenvironment. Genetic ablation of ADAR1 p150 intrinsically inhibits tumor proliferation and extrinsically triggers a robust type I interferon response and profound remodeling of the tumor immune landscape, converting immunologically "cold" tumors to "hot." Furthermore, we establish that myeloid-specific ADAR1 deletion synergizes with anti-PD-1 therapy by enhancing antigen presentation and fostering a pro-inflammatory microenvironment. Crucially, we delineate the Zα domain as the essential structural determinant for dsRNA editing selectivity. Targeted disruption of this domain alone, without affecting the catalytic deaminase domain, is sufficient to recapitulate the potent antitumor effects of complete ADAR1 ablation, leading to accumulation of immunogenic dsRNA, activation of cytosolic sensors (MDA5/PKR), and potent anti-tumor immunity. Our work provides a compelling rationale for selectively targeting the ADAR1 p150-Zα axis to reverse malignant RNA editing and overcome resistance to immunotherapy, offering a refined strategy with a potentially superior therapeutic index.
Published in
Targeting ADAR1 p150 triggers tumor inhibition and antitumor immunity to overcome immunotherapy resistance
Ai ZE, Bian Y, Li G et al. · iScience 2026 · PMID 42221825 · doi:10.1016/j.isci.2026.115978
This dataset
Open GSE316054 in finder → Find more 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 GSE316054_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 PRJNA1400535 and SRA study SRP661019. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 42221825) ↗
Study design
26 conditions, mostly in duplicate
HGC27-788-Adar-N173S-21-IFNB ×2 HGC27-788-Adar-N173S-21-PBS ×2 HGC27-788-IFNB ×2 HGC27-788-PBS ×2 OE21-788-Adar-N173S-2-IFNB ×2 OE21-788-Adar-N173S-2-PBS ×2 OE21-788-IFNB ×2 OE21-788-PBS ×2 +18 more

Supports a between-group comparison across 52 samples.

How we read this: 26 replicated groups read from 52 sample titles; they account for 52 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

+ 12 more — browse all 52 samples with per-sample file links →

Datasets on a similar topic

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