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RSK1-driven TRIM28-E2F1 feedback loop promotes castration-resistant prostate cancer progression

GSE287229 Homo sapiens (human) ChIP-seq / ATAC-seq (genome binding and open chromatin) 15 samples Submitted 2025/06/17 Platform GPL34281
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · human · 15 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
Prostate cancerThis series is part of our curated briefing on it.
Samples
15 samples: 6 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
RSK1-driven TRIM28/E2F1 feedback loop promotes castration-resistant prostate cancer progressionThe Journal of clinical investigation · 2025
Summary (written by the submitters)
Castration-resistant prostate cancer (CRPC) marks the advanced and lethal stage of prostate cancer (PCa). TRIM28, also known as KAP1, is a transcriptional regulator recently shown to promote CRPC cell proliferation and xenograft tumor growth. Nonetheless, knowledge gaps persist regarding the mechanisms underlying TRIM28 upregulation in CRPC as well as the genomic targets regulated by TRIM28.
Read the full summary ↓
Here, we report that TRIM28 is a novel E2F1-target in CRPC. Using an integrated genomic approach, we have demonstrated that TRIM28 forms a positive feedback loop to promote the transcription activation and genomic function of E2F1 independent of Rb status. Furthermore, we identified RSK1 as a kinase that directly phosphorylates TRIM28 at S473, and as such, RSK1 drives the TRIM28-E2F1 feedback loop. Accordingly, pS473-TRIM28 promotes CRPC progression, which is mitigated by RSK inhibition. In summary, our study reveals a critical role of the RSK1–TRIM28–E2F1 axis in CRPC progression, which may be exploited as a vulnerability in treating Rb-deficient CRPC.
Published in
RSK1-driven TRIM28/E2F1 feedback loop promotes castration-resistant prostate cancer progression
Kim M, Liu J, Zhang Y et al. · The Journal of clinical investigation 2025 · PMID 40519166 · doi:10.1172/JCI185119
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 GSE287229_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 PRJNA1211646 and SRA study SRP557901. Searching any of these in the dataset finder brings you back here.

Study design
6 conditions, mostly in duplicate
LN LKO E2F1 ×2 LN shTRIM28 E2F1 ×2 LN shRb E2F1 ×2 LN shRb shTRIM28 E2F1 ×2 WT ATAC ad 2 ×2 473A ATAC ad 2 ×2 TRIM28 LKO CR ad ×1 TRIM28 WT ×1 +1 more

Supports a between-group comparison across 12 samples.

How we read this: 6 replicated groups read from 15 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 Prostate cancer datasets

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