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Tumor-associated Schwann cell remodeling under metabolic stress via lactate sensing orchestrates [ChIP-seq, MeRIP-seq, RNA-seq]

GSE303766 Homo sapiens (human) ChIP-seq / ATAC-seq (genome binding and open chromatin) 36 samples Submitted 2025/08/12 Platform GPL20795Platform GPL24676
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · human · 36 samples

What it is
ChIP-seq / ATAC-seq (genome binding and open chromatin)Where proteins bind the genome, or which regions are open and active.
Organism
Homo sapiens (human)
Topic
Pancreatic cancerThis series is part of our curated briefing on it.
Samples
36 samples: 36 samples, each with a distinct title — no replicated groupsGroups 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)
Diabetes mellitus (DM) is a known risk factor for pancreatic cancer, but the underlying mechanisms remain elusive. Using in vivo models of diabetes-driven pancreatic tumorigenesis and metabolomics analysis, we demonstrate that metabolic stress induced by DM promotes pancreatic cancer progression by remodeling tumor-associated Schwann cells (TASs), impairing CD8+ T cell function.
Read the full summary ↓
We discover that Mettl16+ Cd276+ Nectin2+ Schwann cells play a crucial role in mediating the pro-carcinogenic effects of lactate. Remodeled METTL16+ Schwann cells secret immune evasion factors (CD276, NECTIN2), contributing to anti-PD1 resistance. Furthermore, rosuvastatin was identified in this study as a novel METTL16 inhibitor for pancreatic cancer under metabolic stress. In conclusion, our study underscores the critical role of lactate in the metabolic reprogramming of pancreatic cancer mediated by Schwann cell remodeling, revealing novel pathways for therapeutic intervention.
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 GSE303766_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: Look for peak files (.bed, .narrowPeak) and signal tracks (.bigWig) among the supplementary files; the raw reads are on ENA.

Also filed as BioProject PRJNA1297650 and SRA study SRP603954. Searching any of these in the dataset finder brings you back here.

Study design
36 samples, each with a distinct title — no replicated groups

Any grouping that defines a comparison lives in the sample characteristics, which GEO records separately from the titles.

How we read this: Read from 36 sample titles: 36 distinct titles with little repetition. 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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