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Cancer-associated fibroblast-derived CCL5 promotes cisplatin resistance in neuroendocrine prostate cancer

GSE287963 Mus musculus (mouse) RNA-seq (gene expression) 10 samples Submitted 2025/12/03 Platform GPL24247
At a glance

RNA-seq (gene expression) · mouse · 10 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
10 samples
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
Targeting the CCL5/CCR5 axis in tumor-stromal crosstalk to overcome cisplatin resistance in neuroendocrine prostate cancerJournal of experimental & clinical cancer research : CR · 2025
Summary (written by the submitters)
Chemoresistance remains a significant challenge in the treatment of neuroendocrine prostate cancer (NEPC), a highly aggressive and lethal subtype of prostate cancer. Here, we identify a tumor-stromal interaction mediated by the CCL5/CCR5 signaling axis that drives cisplatin resistance. Cisplatin-induced DNA damage promotes a cGAS-STING–dependent senescence program in cancer-associated fibroblasts (CAFs), resulting in the secretion of CCL5, a key senescence-associated secretory phenotype factor.
Read the full summary ↓
CAF-derived CCL5 binds to CCR5 on tumor cells, promoting the formation of a CCR5/β-arrestin1/p85 complex that activates the PI3K/AKT signaling pathway. This activation enhances DNA repair, protecting tumor cells from cisplatin-induced apoptosis. Pharmacologic inhibition of the CCL5/CCR5 pathway using maraviroc, an FDA-approved CCR5 antagonist, sensitizes NEPC cells to cisplatin treatment and significantly prolongs survival in an NEPC mouse model. These findings establish the CCL5/CCR5 axis as a critical mediator of tumor-stromal crosstalk and provide a promising therapeutic strategy for overcoming chemoresistance in NEPC.
Published in
Targeting the CCL5/CCR5 axis in tumor-stromal crosstalk to overcome cisplatin resistance in neuroendocrine prostate cancer
Liu B, Zhang W, Ji Y et al. · Journal of experimental & clinical cancer research : CR 2025 · PMID 41152972 · doi:10.1186/s13046-025-03552-y
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 GSE287963_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: 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 PRJNA1215370 and SRA study SRP559734. Searching any of these in the dataset finder brings you back here.

Samples in this study

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