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Cell-autonomous IL6ST activation suppresses prostate cancer development via STAT3/ARF/p53-driven senescence and confers an immune-active tumor microenvironment

GSE277063 Mus musculus (mouse) RNA-seq (gene expression) 23 samples Submitted 2024/11/04 Platform GPL19057
At a glance

RNA-seq (gene expression) · mouse · 23 samples

What it is
RNA-seq (gene expression)Gene activity measured by sequencing. The summary does not mention single-cell work, so this is most likely bulk: one average per sample, the usual starting point for comparing groups.
Organism
Mus musculus (mouse)
Samples
23 samples: 8 × prostate epithelial cells, F vs 5 × prostate epithelial cells, B vs 5 × prostate epithelial cells, C vs 5 × prostate epithelial cells, EGroups 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
Cell-autonomous IL6ST activation suppresses prostate cancer development via STAT3/ARF/p53-driven senescence and confers an immune-active tumor microenvironmentMolecular cancer · 2024
Summary (written by the submitters)
Prostate cancer ranks as the second most frequently diagnosed cancer in men worldwide. Recent research highlights the crucial roles IL6ST-mediated signaling pathways play in the development and progression of various cancers, particularly through hyperactivated STAT3 signaling. Here, we find that genetic cell-autonomous activation of the IL6ST receptor in prostate epithelial cells triggers active STAT3 signaling and significantly reduces tumor growth in vivo.
Read the full summary ↓
Mechanistically, genetic activation of IL6ST signaling mediates senescence via the STAT3/ARF/p53 axis and anti-tumor immunity via recruitment of cytotoxic T-cells, ultimately impeding tumor progression. Our findings reveal a context-dependent role of IL6ST/STAT3 in carcinogenesis and a tumor-suppressive function in prostate cancer development. We challenge the prevailing concept of blocking IL6ST/STAT3 signaling as functional prostate cancer treatment and instead propose cell-autonomous IL6ST activation as a novel therapeutic strategy.
Published in
Cell-autonomous IL6ST activation suppresses prostate cancer development via STAT3/ARF/p53-driven senescence and confers an immune-active tumor microenvironment
Sternberg C, Raigel M, Limberger T et al. · Molecular cancer 2024 · PMID 39482716 · doi:10.1186/s12943-024-02114-8
This dataset
Open GSE277063 in finder → Find more mouse RNA-seq datasets →
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 GSE277063_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: For RNA-seq the counts are usually a table among the supplementary files (look for 'counts', 'expression', 'FPKM' or 'TPM' in the file name). The series matrix of a sequencing study is sometimes nearly empty.

Also filed as BioProject PRJNA1160310 and SRA study SRP532364. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 39482716) ↗
Study design
8 × prostate epithelial cells, F vs 5 × prostate epithelial cells, B vs 5 × prostate epithelial cells, C vs 5 × prostate epithelial cells, E

Supports a between-group comparison across 23 samples.

How we read this: 4 replicated groups read from 23 sample titles; they account for 23 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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