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Starvation induced circulating miR-33a secretion remodeled extracellular matrix of tumor microenvironment by altering polyamine metabolism [CAF EV]

GSE222292 Homo sapiens Expression profiling by high throughput sequencing 6 samples Submitted 2025/08/01 Platform GPL24676
Summary
Breast cancer cells secret different kinds of cargoes through extracellular vesicles (EVs) especially under stress conditions. However, the underling mechanism and function is poorly defined. Here, we found RNA binding protein ACO1 could bind miR-33a and assist their package into EVs in tumor core region. Thereby, miR-33a suppressed putrescine metabolism in cancer-associated fibroblasts (CAFs) and reprogrammed H3K4me3 mediated epigenetic regulation. Chip-seq data suggested stress granules related genes were downregulated and ECM related genes were upregulated. Most notably, putrescine inhibited KDM5C expression level but did not altered activity. Finally, our study provides a novel mechanism of how cancer EVs reprogrammed polyamine metabolism in tumor stroma, leading to spatially different distribution of ECM in tumor microenvironment.
Published in
Cancer Cell-Secreted miR-33a Reduces Stress Granule Formation by Targeting Polyamine Metabolism in Stroma to Promote Tumourigenesis
Hu S, Li X, Hu Q et al. · Journal of extracellular vesicles 2025 · PMID 40903826 · doi:10.1002/jev2.70153
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Also filed as BioProject PRJNA919174 and SRA study SRP416327. Searching any of these in the dataset finder brings you back here.

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