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Updated: Jan 12, 2026

Advancements in the Metabolic Profiling of Three-Dimensional Brain Tumor Spheroids for Drug Screening
Published on: September 5, 2025
Tau impedes glioma progression by enhancing fatty acid β-oxidation-induced cellular senescence
Wan-Hong Han1, Wu-Jie Zhao1, Jia-Wei He1
1Department of Neurosurgery and Department of Neuroscience, Fujian Key Laboratory of Brain Tumors Diagnosis and Precision Treatment, Xiamen Key Laboratory of Brain Center, the First Affiliated Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen, Fujian 361102, China.
Abstract:
Tau ( MAPT) expression is inversely associated with glioma malignancy and patient survival. However, the molecular mechanisms underlying this correlation are yet to be fully investigated. This study demonstrated that tau suppressed glioma cell proliferation both in vitro and in vivo. Mechanistically, tau promoted fatty acid β-oxidation, leading to DNA damage and glioma cellular senescence. Functional analyses revealed that tau interacted with carnitine palmitoyltransferase 1A (CPT1A), enhancing CPT1 enzymatic activity and thereby accelerating lipid catabolism. These findings establish tau as a regulator of metabolic reprogramming and senescence in glioma via CPT1-dependent β-oxidation and support its potential as a therapeutic target in glioma management.
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