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Transcriptome changes associated with targeting mTORC1 in endothelial cells

GSE256509 Mus musculus Expression profiling by high throughput sequencing 8 samples Submitted 2024/04/01 Platform GPL28457
Summary
Tumor metastasis, the main cause of death in cancer patients, requires outgrowth of tumor cells after their dissemination and residence in microscopic niches. Nutrient sufficiency is a determinant of such outgrowth. Fatty acids (FA) can be metabolized by cancer cells for their energetic and anabolic needs, thereby supporting metastatic progression. The vascular endothelium serves as a barrier to access of molecules into tissues, but it is unclear how fatty acid delivery to early metastatic tumors is regulated. Using a mouse model of metastatic outgrowth in the lung, we show that tumor endothelium actively promotes tumor growth by transferring FA into developing metastatic tumors. Tumor burden was significantly reduced upon endothelial-specific targeted deletion of Raptor, a unique component of the mTORC1 complex (RptorECKO). The goal of this study was to investigate how targeting Raptor/mTORC1 impacts endothelial cells.
Published in
Increased fatty acid delivery by tumor endothelium promotes metastatic outgrowth
Edwards DN, Wang S, Kane K et al. · JCI insight 2025 · PMID 40198126 · doi:10.1172/jci.insight.187531
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Also filed as BioProject PRJNA1079803 and SRA study SRP491430. Searching any of these in the dataset finder brings you back here.

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