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Targeting CPT1A triggers cGAS/STING activation to engage neutrophils for tumor elimination

GSE289953 Mus musculus Expression profiling by high throughput sequencing 3 samples Submitted 2026/02/18 Platform GPL19057
Summary
Lipid metabolism plays an important role in tumor progression and immune evasion. Targeting fatty acid oxidation (FAO) has been shown to be a promising approach to treat cancers. However, the impact of FAO inhibition on tumor immune microenvironment is still less understood. In this study, we found that inhibiting FAO by targeting CPT1A dramatically triggers cGAS/STING activation through inducing cytoplasmic leakage of mitochondrial DNA. This leads to the infiltration of neutrophils into tumors and drive anti-tumor effects of a subset of neutrophils, which plays a crucial role in inhibiting tumor growth. Our current findings suggest that CPT1A could be a promising target for TNBC therapy and, moreover, we uncover an essential anti-tumor role of neutrophils upon cGAS/STING activation.
Published in
Inhibition of CPT1A activates the cGAS/STING pathway to enhance neutrophil-mediated tumor abrogation in triple-negative breast cancer
Li C, Gao T, Zhao Q et al. · Cancer letters 2025 · PMID 40825468 · doi:10.1016/j.canlet.2025.217991
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Also filed as BioProject PRJNA1225629 and SRA study SRP564947. Searching any of these in the dataset finder brings you back here.

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