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S-nitrosylation of IRF7 induced by NOS1 expression in Melanoma suppresses anti-tumor immunity

GSE279140 Mus musculus (mouse) RNA-seq (gene expression) 12 samples Submitted 2025/10/01 Platform GPL24247
At a glance

RNA-seq (gene expression) · mouse · 12 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
12 samples: 3 × WTCTRL vs 3 × MUTCTRL vs 3 × WTIFN vs 3 × MUTIFNGroups 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)
Endogenous nitric oxide (NO) produced by nitric oxide synthases (NOSs) plays an important immunosuppressive role in the tumor microenvironment. In melanoma, NOS1 expression was increased with tumor progression and correlated with tumor immune escape through inhibition on type I interferon (IFN) signaling. However, the immune regulatory role and its related mechanism of NOS1 and its impacts on immune therapy such as immune checkpoint blockade (ICB) in melanoma is unclear.
Read the full summary ↓
Here, we found that NOS1 expression induced IRF7 modification by s-nitrosylation at C435 site in mouse (C481 in human), which functionally promotes tumor growth in mouse models. Mechanically, IRF7-C435-SNO inhibited IFNβ transcription under PRR signal activation, leading to disorder in initiation of type I interferons response in melanoma cell. In melanoma mouse model, IRF7-C435-SNO decreased infiltration and activation of CD8 T cells in tumor microenvironment, by reducing antigen presentation processes in tumor cells and inhibits the maturation of DC1. Clinically, high expression of NOS1 correlated with poor survival prognosis and resistance with to ICB anti-tumor therapies in melanoma cases with less immune cell infiltration. Our study suggested that NOS1 expression in melanoma characterizes IFN-I signal disorders in response to innate immune stimulation by IRF7 s-nitrosylation. Targeting NOS1 signaling might benefit for overcome of immune therapeutically resistance particularly in immune cold melanoma phenotype.
This dataset
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.

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 GSE279140_RAW.tar (it can run to tens of gigabytes).

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.

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 PRJNA1170966 and SRA study SRP537541. Searching any of these in the dataset finder brings you back here.

Study design
3 × WTCTRL vs 3 × MUTCTRL vs 3 × WTIFN vs 3 × MUTIFN

Supports a between-group comparison across 12 samples.

How we read this: 4 replicated groups read from 12 sample titles; they account for 12 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
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