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Implantation of engineered adipocytes that outcompete tumors for resources suppresses cancer progression

GSE246231 Homo sapiens (human) RNA-seq (gene expression) 17 samples Submitted 2024/10/17 Platform GPL24676
At a glance

RNA-seq (gene expression) · human · 17 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)
Samples
17 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
Implantation of engineered adipocytes suppresses tumor progression in cancer modelsNature biotechnology · 2025
Summary (written by the submitters)
Tumors acquire an increased ability to obtain and metabolize nutrients. Here, we engineered adipocytes to outcompete tumors for nutrients and show that they can substantially reduce cancer progression. Growing cells from several cancers (breast, colon, pancreas, prostate) with engineered human adipocytes or xenografts alongside adipose organoids significantly suppresses cancer progression and reduces hypoxia and angiogenesis.
Read the full summary ↓
Transplanting modulated adipocyte organoids in pancreatic or breast cancer genetic mouse models significantly suppressed their growth and decreased angiogenesis and hypoxia. To further showcase therapeutic potential, we demonstrate that co-culturing engineered patient-derived adipocytes with tumor organoids from dissected human breast cancers significantly reduces cancer growth and reduces proliferation of organoids from donors with BRCA1/2 mutations. In addition, inducing adipose organoids to outcompete tumors via tetracycline or placing them in an integrated cell-scaffold delivery platform and implanting them next to the tumor, both significantly suppress cancer growth. Finally, to display how this approach can be customized for different tumor-associated metabolic programs, we show that upregulating UPP1 in adipose organoids can outcompete a uridine-dependent pancreatic ductal adenocarcinoma for resources and suppress its growth. Combined, our results introduce a novel cancer therapeutic approach, termed adipose modulation transplantation (AMT), that can be utilized for a broad range of cancers.
Published in
Implantation of engineered adipocytes suppresses tumor progression in cancer models
Nguyen HP, An K, Ito Y et al. · Nature biotechnology 2025 · PMID 39905264 · doi:10.1038/s41587-024-02551-2
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 GSE246231_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 PRJNA1032093 and SRA study SRP468423. Searching any of these in the dataset finder brings you back here.

Samples in this study

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+ 17 more — browse all 17 samples with per-sample file links →

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