Tau impedes glioma progression via enhancing fatty acid ß-oxidation induced cellular senescence
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 ß-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. Overall design: U87 cell which overexpresdsed control vector or tau were used forRNA-Seq analysis to identify tau induced different genes