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NAT10 promotes cancer metastasis by modulating p300/CBP activity through chromatin-associated tRNA [ChIP-seq]

GSE250428 Mus musculus (mouse) ChIP-seq / ATAC-seq (genome binding and open chromatin) 23 samples Submitted 2025/11/17 Platform GPL24247
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · mouse · 23 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
Mus musculus (mouse)
Samples
23 samples: 8 conditions, mostly in duplicateGroups 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
NAT10 promotes cancer metastasis by modulating p300/CBP activity through chromatin-associated tRNAMolecular cell · 2025
Summary (written by the submitters)
Acetylation of proteins and RNA is crucial for development and cancer progression. NAT10 is the sole RNA acetylase responsible for N4-acetylcytidine (ac4C) modification of various RNAs. Our study reveals that NAT10 loss significantly reduces lung metastasis in breast cancer mouse models. NAT10 interacts with a mechanosensitive, metastasis-susceptibility protein complex at the nuclear pore.
Read the full summary ↓
Mechanistically, NAT10-mediated acetylation of chromatin-associated tRNAs enhances p300/CBP activity. Without NAT10, acetylation of these tRNAs decreases, leading to p300/CBP inactivation and mislocalization. As a result, NAT10 depletion disrupts enhancer organization, altering gene transcription critical for metastasis, including reduced chemokines that recruit myeloid cells and create a less metastasis-prone tumor microenvironment. Our findings highlight the distinct role of NAT10 in acetylated tRNA-dependent regulation of enhancer function in metastatic tumor cells and its impact on tumor-immune interactions influencing metastasis.
Published in
NAT10 promotes cancer metastasis by modulating p300/CBP activity through chromatin-associated tRNA
Amin R, Ha NH, Qiu T et al. · Molecular cell 2025 · PMID 41344331 · doi:10.1016/j.molcel.2025.11.010
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 GSE250428_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 PRJNA1054053 and SRA study SRP478598. Searching any of these in the dataset finder brings you back here.

Study design
8 conditions, mostly in duplicate
H3K27ac_WT biol ×2 H3K27ac_KO biol ×2 H4K20ac_WT biol ×2 H4K20ac_KO biol ×2 H3K27me3_WT biol ×2 H3K27me3_KO biol ×2 Input_WT biol ×2 Input_KO biol ×2 +7 more

Supports a between-group comparison across 16 samples.

How we read this: 8 replicated groups read from 23 sample titles; they account for 16 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
Datasets on a similar topic

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