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Probiotics Complex Synergizes with FOLFOX to Enhance Antitumor Response and Ameliorate Chemotherapy-induced Intestinal Toxicity via Upregulation of NAD+ Metabolism

GSE311912 Mus musculus (mouse) RNA-seq (gene expression) 27 samples Submitted 2026/06/01 Platform GPL24247
At a glance

RNA-seq (gene expression) · mouse · 27 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
27 samples: 5 conditions, mostly with about 5 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.
Summary (written by the submitters)
Modulating the gut microbiota can improve chemotherapy efficacy, but strategies that simultaneously reduce toxicity and enhance therapeutic outcomes remain understudied. This study developed a NAD⁺-enhanced composite probiotic formulation (derived from fermented yak milk from the Qinghai-Tibet Plateau) to alleviate FOLFOX-induced intestinal toxicity and enhance efficacy in a colitis-associated colorectal cancer (CAC) mouse model.
Read the full summary ↓
Metabolomics revealed significant contributions of nicotinic acid and nicotinamide metabolism to the body's response to chemotherapy. Consequently, RNA-seq was employed to validate the criticality of nicotinamide metabolism at the gene expression level: probiotics counteracted FOLFOX-induced NAD⁺ depletion, restored SIRT1/3 activity, and suppressed FoxO3a-mediated chemotherapy resistance. A clinical cohort of 53 gastrointestinal cancer patients confirmed serum NAD⁺ levels correlate with gut microbiota and intestinal toxicity. Collectively, we propose a microbiota-targeting strategy synergizing with FOLFOX, providing a translatable paradigm for precision oncology.
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 GSE311912_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 PRJNA1371933 and SRA study SRP650180. Searching any of these in the dataset finder brings you back here.

Study design
5 conditions, mostly with about 5 replicates each
Negative control, A ×6 CAC_FPL, H ×6 CAC, B ×5 CAC_F, F ×5 CAC_FP, G ×5

Supports a between-group comparison across 27 samples.

How we read this: 5 replicated groups read from 27 sample titles; they account for 27 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.