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Acetylcyssteine synergizes PD-1 blockers against colorectal cancer progression by promoting TCF1+PD1+CD8+ T cell differentiation in mice

GSE252358 Mus musculus (mouse) RNA-seq (gene expression) 10 samples Submitted 2024/05/23 Platform GPL24247
At a glance

RNA-seq (gene expression) · mouse · 10 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
10 samples: 5 × C vs 5 × NGroups 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)
PD-1 blockade is important in treating progressive colorectal cancer (CRC). However, some patients with CRC have a poor or no response to immunotherapy. An important reason for this problem is the exhaustion of CD8+ T cells in the tumor microenvironment. Acetylcysteine (NAC) can reduce CD8+ T cell exhaustion in vitro and induce their differentiation into long-lasting phenotypes, thus enhancing the anti-tumor effect of adoptive T cell transfer.
Read the full summary ↓
However, whether NAC can be combined with PD-1 blockade in CRC treatment and how NAC regulates CD8+ T cell differentiation remains unclear. We constructed a mouse CRC model to study the effect of NAC on tumors. The effect of NAC on CD8+ T cell differentiation and its potential mechanism were explored by cell flow assay and other studies in vitro and ex vivo. We demonstrated that NAC synergized PD-1 antibodies to inhibit CRC progression in a mouse CRC model, mediated by CD8+ T cells. NAC induces TCF1+PD1+CD8+ T cell differentiation and reduces the formation of exhausted T cells (Tex). Moreover, NAC enhanced the expression of Glut4 in CD8+ T cells, promoting the differentiation of TCF1+PD1+CD8+ T cells. Our study provides a novel idea for immunotherapy of clinically progressive CRC and suggests that Glut4 may be a new immunometabolic molecular target for regulating CD8+ T cell differentiation.
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 GSE252358_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 PRJNA1060282 and SRA study SRP480912. Searching any of these in the dataset finder brings you back here.

Study design
5 × C vs 5 × N

Supports a between-group comparison across 10 samples.

How we read this: 2 replicated groups read from 10 sample titles; they account for 10 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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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.