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Human bone marrow adipocytes drive prostate cancer bone metastasis progression via lipid-mediated induction of Angiopoietin-like 4

GSE312982 Homo sapiens (human) RNA-seq (gene expression) 10 samples Submitted 2025/12/16 Platform GPL18573
At a glance

RNA-seq (gene expression) · human · 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
Homo sapiens (human)
Topic
Prostate cancerThis series is part of our curated briefing on it.
Samples
10 samples: 5 × PC3 non cocultivated vs 5 × PC3 cocultivatedGroups 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.
Summary (written by the submitters)
Bone is the predominant metastatic site in advanced prostate cancer (PCa), and the role of bone marrow adipocytes (BMAds) which constitute over 70% of adult marrow remains poorly understood. Herein, we developed a physiologically relevant 3D culture model using primary human BMAds from red hematopoietic rich-areas (rBMAds). Using this model, we show that rBMAds engage in metabolic crosstalk with PCa cells by releasing free fatty acids (FFAs) through a non-canonical lipolytic pathway.
Read the full summary ↓
These FFAs are taken up by PCa cells, and induce a transcriptional reprogramming that promotes motility. Among the responsive genes, Angiopoietin like 4 (ANGPTL4) is the most upregulated via a Peroxisome proliferator-activated receptor γ (PPARγ)-dependent mechanism, and its silencing abolishes the rBMAd-driven migratory and invasive phenotype. In bone metastases of patients with PCa, high ANGPTL4 levels correlated with poor survival. Together, our findings uncover a novel adipocyte-tumor interaction and identify ANGPTL4 as a key mediator and potential therapeutic target in bone-metastatic PCa.
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 GSE312982_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 PRJNA1378047 and SRA study SRP653662. Searching any of these in the dataset finder brings you back here.

Study design
5 × PC3 non cocultivated vs 5 × PC3 cocultivated

Supports a between-group comparison across 10 samples.

How we read this: 2 replicated groups read from 10 sample titles; they account for 10 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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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.