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Tau impedes glioma progression via enhancing fatty acid β-oxidation induced cellular senescence

GSE294870 Homo sapiens Expression profiling by high throughput sequencing 6 samples Submitted 2025/12/01 Platform GPL24676
Summary
Tau (MAPT) gene and protein levels exhibit a negative correlation with glioma malignancy and reduced survival rates. However, the molecular mechanisms underlying this correlation require to be further investigated. In this study, we observed tau impedes glioma cell growth both in vitro and in vivo. Mechanistically, tau enhanced fatty acid β-oxidation, which induces DNA damage and glioma cellular senescence. Furthermore, we identified that the molecular mechanism by which tau regulates lipid metabolism is its binding to CPT1A and promoting CPT1 activity. Our findings highlight the biological role of tau in regulating lipid metabolism and cellular senescence in a CPT1 activity-dependent manner. These results suggest that tau may serve as a promising therapeutic target for glioma in the future.
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Also filed as BioProject PRJNA1251890 and SRA study SRP579341. Searching any of these in the dataset finder brings you back here.

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