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USP11 promotes prostate cancer progression by upregulating AR and c-Myc activity [CUT&RUN]

GSE268252 Homo sapiens (human) ChIP-seq / ATAC-seq (genome binding and open chromatin) 26 samples Submitted 2024/07/13 Platform GPL24676
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · human · 26 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
26 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
USP11 promotes prostate cancer progression by up-regulating AR and c-Myc activityProceedings of the National Academy of Sciences of the United States of America · 2024
Summary (written by the submitters)
Androgen receptor (AR) is a main driver for castration-resistant prostate cancer (CRPC). c-Myc is an oncogene underlying prostate tumorigenesis. Here we find that the deubiquitinase USP11 targets both AR and c-Myc in prostate cancer. USP11 expression was upregulated in metastatic prostate cancer and CRPC. USP11 knockdown significantly inhibited prostate cancer cell growth.
Read the full summary ↓
Our RNA-seq studies revealed AR and c-Myc as the top transcription factors altered after USP11 knockdown. ChIP-seq analysis showed that either USP11 knockdown or replacement of endogenous USP11 with a catalytic-inactive USP11 mutant significantly decreased chromatin binding by AR and c-Myc. We find that USP11 employs two mechanisms to upregulate AR and c-Myc levels: namely, deubiquitination of AR and c-Myc proteins to increase their stability; deubiquitination of H2A-K119Ub, a repressive histone mark, on promoters of AR and c-Myc genes to increase their transcription. AR and c-Myc re-expression in USP11-knockdown prostate cancer cells partly rescued cell growth defects. Thus, our studies reveal a tumor-promoting role for USP11 in aggressive prostate cancer through upregulation of AR and c-Myc activities and support USP11 as a potential target against prostate cancer.
Published in
USP11 promotes prostate cancer progression by up-regulating AR and c-Myc activity
Pornour M, Jeon HY, Ryu H et al. · Proceedings of the National Academy of Sciences of the United States of America 2024 · PMID 39052835 · doi:10.1073/pnas.2403331121
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 GSE268252_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 PRJNA1115793 and SRA study SRP509537. Searching any of these in the dataset finder brings you back here.

Study design
8 conditions, mostly in duplicate
RV1, pLKO.1, AR, ×2 RV1, USP11-KD, AR, ×2 RV1, pLKO.1, c-Myc, ×2 RV1, USP11-KD, c-Myc, ×2 Rv1, pLvx, HA, ×2 Rv1, USP11-WT, HA-USP11, ×2 Rv1, USP11-CS, HA-USP11, ×2 RV1, USP11-CS, c-Myc, ×2 +10 more

Supports a between-group comparison across 16 samples.

How we read this: 8 replicated groups read from 26 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
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