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Adrenal-derived factors drive progression of sclerotic prostate cancer in bone

GSE333317 Homo sapiens (human) RNA-seq (gene expression) 48 samples Submitted 2026/05/31 Platform GPL24247Platform GPL24676
At a glance

RNA-seq (gene expression) · human · 48 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
Homo sapiens (human)
Topic
Prostate cancerThis series is part of our curated briefing on it.
Samples
48 samples: 48 samples, each with a distinct title — no replicated groupsGroups 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
Adrenal-derived factors drive progression of sclerotic prostate cancer in boneEndocrine-related cancer · 2026
Summary (written by the submitters)
Bone metastasis is a leading cause of death in prostate cancer (PC) patients. Although androgen‐deprivation therapy (ADT) combined with novel androgen‐targeted agents constitutes the cornerstone of systemic treatment, its efficacy is limited. We investigated the adrenal contribution in promoting progression of castration-resistant PC (CRPC) within bone using a preclinical intratibial xenograft model (VCaP, 22Rv1, and LNCaP cells).
Read the full summary ↓
Mice underwent orchiectomy (ORX) to mimic ADT, with or without adrenalectomy (ORX+ADX) to eliminate adrenal contribution. A significant increase in bone mineral density (BMD) was observed in tumor-grafted tibiae in ORX-treated mice compared to controls (p<0.001), indicating a strong tumor-induced sclerotic response. In contrast, ORX+ADX reduced tumor take rate by approximately 50% and decreased tumor-induced BMD by over 80% (p<0.001). Transcriptomic analysis revealed that ADX downregulated tumor-induced transcripts in bone by over 90%, including osteogenic (Lox, Sparcl1, Bmp2, Postn, Col1a1) and pro-angiogenic (Bmper, Pecam-1, Esam) signatures. Additionally, BMP, PI3K/Akt and ERK1/2 signaling pathways were associated with the tumor-induced bone response. Both high serum progesterone and intratumoral levels of dihydrotestosterone (DHT) were associated with the sclerotic bone phenotype. ADX markedly reduced intratumoral DHT and downregulated glycolytic genes (HK2, PFK2, LDHA) and secretory proteins expressed by the tumor, including Stanniocalcin 2, potentially mediating paracrine effects in the sclerotic bone response. Altogether, these findings highlight the critical role of adrenal- dependent androgen synthesis, particularly via progesterone, in driving the sclerotic CRPC in bone. Our findings suggest that a comprehensive blockade of adrenal contribution is essential to prevent the sclerotic bone response associated with CRPC.
Published in
Adrenal-derived factors drive progression of sclerotic prostate cancer in bone
Hagberg Thulin M, Li L, Abrahamsson S et al. · Endocrine-related cancer 2026 · PMID 42149634 · doi:10.1530/ERC-25-0309
This dataset
Open GSE333317 in finder → Find more RNA-seq datasets → Prostate cancer landscape →
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 GSE333317_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 PRJNA1470657 and SRA study SRP703816. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 42149634) ↗
Study design
48 samples, each with a distinct title — no replicated groups

Any grouping that defines a comparison lives in the sample characteristics, which GEO records separately from the titles.

How we read this: Read from 48 sample titles: 48 distinct titles with little repetition. 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

+ 8 more — browse all 48 samples with per-sample file links →

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Metadata from NCBI GEO, cached and refreshed periodically — the NCBI page above is authoritative. Downloads link straight to NCBI/ENA; nothing is proxied through BioTransfer.