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Cancer cell intrinsic SSBP4 enables tumor immune evasion by promoting cholesterol biosynthesis [RNA-Seq]

GSE328719 Mus musculus (mouse) RNA-seq (gene expression) 15 samples Submitted 2026/04/30 Platform GPL24247
At a glance

RNA-seq (gene expression) · mouse · 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
Mus musculus (mouse)
Samples
15 samples: 4 × RNA-Seq, MC38, SSBP4 WT, vs 4 × RNA-Seq, B16-F10, SSBP4 WT, vs 4 × RNA-Seq, B16-F10, SSBP4 KO, vs 3 × RNA-Seq, MC38, SSBP4 OE,Groups 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
Cancer Cell-Intrinsic SSBP4 Enables Tumor Immune Evasion by Promoting Cholesterol BiosynthesisCancer immunology research · 2026
Summary (written by the submitters)
The immunosuppressive tumor microenvironment (TME) contributes to resistance against checkpoint inhibitors. However, the precise factors that shape the immune contexture of the TME remain elusive. Here, we report that Single-Stranded DNA Binding Protein 4 (SSBP4), a previously uncharacterized protein, suppresses intratumoral T-cell activation by promoting excessive cholesteryl ester production in tumor cells.
Read the full summary ↓
Overexpression of SSBP4 in tumor cells decreased T-cell infiltration and accelerated tumor growth in murine syngeneic tumor models. Conversely, genetic ablation of SSBP4 in tumor cells enhanced T-cell infiltration and inhibited tumor growth in a CD8+ T cell–-dependent manner. Mechanistically, SSBP4 upregulated cholesterol synthesis genes, leading to increased production of cholesterol and cholesteryl esters in tumor cells, which directly suppressed CD8+ T-cell activation and function. Furthermore, SSBP4 abrogation significantly improved the efficacy of anti-PD-1 treatment. Thus, in this study, we have identified SSBP4 as a cancer cell–intrinsic regulator of cholesterol metabolism that contributes to tumor immune evasion.
Published in
Cancer Cell-Intrinsic SSBP4 Enables Tumor Immune Evasion by Promoting Cholesterol Biosynthesis
Ou P, Eres I, Zhao J et al. · Cancer immunology research 2026 · PMID 42054532 · doi:10.1158/2326-6066.CIR-25-1312
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 GSE328719_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 PRJNA1456417 and SRA study SRP693845. Searching any of these in the dataset finder brings you back here.

Study design
4 × RNA-Seq, MC38, SSBP4 WT, vs 4 × RNA-Seq, B16-F10, SSBP4 WT, vs 4 × RNA-Seq, B16-F10, SSBP4 KO, vs 3 × RNA-Seq, MC38, SSBP4 OE,

Supports a between-group comparison across 15 samples.

How we read this: 4 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
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