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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: BACKGROUND, METHODS, RESULTS. Meshes: Animals, Blotting, Western, Brain Neoplasms, Cell Line, Tumor, Cell Proliferation, Disease Progression, Gene Expression Regulation, Enzymologic, Gene Expression Regulation, Neoplastic, Glioma, Glycogen Synthase Kinase 3, Glycogen Synthase Kinase 3 beta, Humans, Hypoxia-Inducible Factor 1, alpha Subunit, Male, Mice, Inbred BALB C, Mice, Nude, Neovascularization, Pathologic, Phosphorylation, Ribosomal Protein S6 Kinases, 70-kDa, Signal Transduction, TOR Serine-Threonine Kinases, Tissue Array Analysis, Transfection, Vascular Endothelial Growth Factor A, beta Catenin.
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Does gSK-3β regulate tumor growth and angiogenesis in human glioma cells? Context: Glioma accounts for the majority of primary malignant brain tumors in adults. Glioma specimens and normal brain tissues were analyzed for the expression levels of GSK-3β and p-GSK-3β (Ser9) by tissue microarray analysis (TMA) and Western blotting. Glioma cells over-expressing GSK-3β were used to analyze biological functions both in vitro and in vivo. The levels of p-GSK-3β (Ser9), but not total GSK-3β, are significantly up-regulated in glioma tissues compared to normal tissues, and are significantly correlated with the glioma grades. Ectopic expression of GSK-3β decreased the phosphorylation levels of mTOR and p70S6K1; and inhibited β-catenin, HIF-1α and VEGF expression. Forced expression of GSK-3β in glioma cells significantly inhibited both tumor growth and angiogenesis in vivo.
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These results reveal that GSK-3β regulates mTOR/p70S6K1 signaling pathway and inhibits glioma progression in vivo; its inactivation via p-GSK-3β (Ser9) is associated with glioma development, which is new mechanism that may be helpful in developing GSK-3β-based treatment of glioma in the future. Final Decision: yes