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E2F4/SETD1A axis-mediated METTL3 methylation promotes tumor immune evasion through impeding endogenous retroelements expression

GSE296929 Homo sapiens (human) DNA methylation 18 samples Submitted 2025/12/01 Platform GPL29480
At a glance

DNA methylation · human · 18 samples

What it is
DNA methylationChemical marks on DNA that help switch genes on or off.
Organism
Homo sapiens (human)
Topic
Colorectal cancerThis series is part of our curated briefing on it.
Samples
18 samples: 6 × LoVo METTL3 WT vs 6 × LoVo METTL3 K513Groups 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)
Colorectal cancer (CRC) progression and recurrence persist as major clinical challenges despite standard therapies. Emerging evidence underscores that tumor relapse arises from crosstalk between malignant cells and the immunosuppressive microenvironment, yet the role of non-histone lysine methylation in this interplay remains unclear.
Read the full summary ↓
Here, we identify di-methylation of lysine 513 (K513) on methyltransferase-like 3 (METTL3) as a key epigenetic modification associated with CRC progression and recurrence. Mechanistically, we reveal that SETD1A catalyzes METTL3 K513 methylation, enhancing its binding affinity to S-adenosylmethionine (SAM) and augmenting RNA m⁶A deposition. Strikingly, METTL3 methylation suppresses endogenous retroelements expression, leading to impaired type I interferon responses and tumor immune evasion. We further uncover a fluorouracil-induced E2F4/SETD1A/METTL3 regulatory axis, wherein E2F4 self-regulation activates SETD1A to drive METTL3 methylation. Targeting this axis through pharmacological inhibition of E2F4 or genetic disruption of METTL3 methylation synergizes with immune checkpoint blockade (ICB), significantly suppressing tumor growth. Our findings unveil a methylation-dependent regulatory mechanism that reshapes the tumor immune microenvironment, offering a novel therapeutic strategy for CRC.
This dataset
Open GSE296929 in finder → Find more human methylation datasets → Colorectal cancer landscape →
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.

Series matrix ↓
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 GSE296929_RAW.tar (it can run to tens of gigabytes).

All supplementary files ↗ Whole study · RAW.tar ↓
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.

Raw reads on ENA ↗

What the files usually look like: Look for beta-value tables or raw IDAT files among the supplementary files.

Also filed as BioProject PRJNA1261950 and SRA study SRP584649. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗
Study design
6 × LoVo METTL3 WT vs 6 × LoVo METTL3 K513

Supports a between-group comparison across 12 samples.

How we read this: 2 replicated groups read from 18 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
More Colorectal cancer datasets

Search all human methylation datasets in GEO →

Share this dataset

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.