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ZC3H13 Loss Drives Cancer Metastatic Progression by Disrupting m6A RNA Methylation

GSE309246 Homo sapiens (human) DNA methylation 12 samples Submitted 2025/09/30 Platform GPL24676
At a glance

DNA methylation · human · 12 samples

What it is
DNA methylationChemical marks on DNA that help switch genes on or off.
Organism
Homo sapiens (human)
Samples
12 samples: 3 × BPH1 dCas9 vs 3 × BPH1 Empty_Vector vs 3 × BPH1 ZC3H13 OE vs 3 × BPH1 ZC3H13 KOGroups 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
ZC3H13 Loss Drives Cancer Metastatic Progression by Disrupting m6A RNA MethylationCancer research · 2026
Summary (written by the submitters)
Aggressive metastatic cancer remains a major clinical challenge due to the unclear underlying mechanisms and the limited treatment options available. N6-methyladenosine (m6A) is a reversible modification of RNA that is frequently altered in cancer, and inhibitors targeting regulators of this process have been shown to block tumorigenesis.
Read the full summary ↓
A better understanding of the role of m6A modifications in driving metastatic properties could help reveal potential strategies to prevent and treat metastasis. In this study, we discovered loss of the m6A writer complex component ZC3H13 as a key regulator of metastatic progression. Co-loss of ZC3H13 together with RB1 and BRCA2 occurred in patients with metastatic prostate cancer. Functional in vitro and in vivo assays demonstrated that ZC3H13 loss changes m6A writer complex activity and target specificity, leading to decreased m6A methylation and increased stability of transcripts that promote migration and invasion. Treatment with FDA-approved m6A demethylase inhibitors effectively reduced the metastatic capabilities of ZC3H13-deficient cells. Together, these findings provide insights into how the m6A writer complex selectively methylates mRNAs, highlight the pathological consequences of altered writer complex composition in cancer, and reveal therapeutic avenues for patients with metastatic cancer.
Published in
ZC3H13 Loss Drives Cancer Metastatic Progression by Disrupting m6A RNA Methylation
Monteagudo-García Ó, Nombela P, Román ÁC et al. · Cancer research 2026 · PMID 41105668 · doi:10.1158/0008-5472.CAN-24-3975
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 GSE309246_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 beta-value tables or raw IDAT files among the supplementary files.

Also filed as BioProject PRJNA1334414 and SRA study SRP627371. Searching any of these in the dataset finder brings you back here.

Study design
3 × BPH1 dCas9 vs 3 × BPH1 Empty_Vector vs 3 × BPH1 ZC3H13 OE vs 3 × BPH1 ZC3H13 KO

Supports a between-group comparison across 12 samples.

How we read this: 4 replicated groups read from 12 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
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