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In glioblastoma-derived cell lines, PTEN does not significantly alter apoptotic sensitivity or cause complete inhibition of DNA synthesis. However, in these cell lines PTEN regulates hypoxia- and IGF-1-induced angiogenic gene expression by regulating Akt activation of HIF-1 activity. Restoration of wild-type PTEN to glioblastoma cell lines lacking functional PTEN ablates hypoxia and IGF-1 induction of HIF-1-regulated genes. In addition, Akt activation leads to HIF-1alpha stabilization, whereas PTEN attenuates hypoxia-mediated HIF-1alpha stabilization. We propose that loss of PTEN during malignant progression contributes to tumor expansion through the deregulation of Akt activity and HIF-1-regulated gene expression.


Journal article


Genes Dev

Publication Date





391 - 396


Apoptosis, Brain Neoplasms, Cell Hypoxia, Culture Media, Serum-Free, Cyclooxygenase 1, DNA-Binding Proteins, Disease Progression, Endothelial Growth Factors, Gene Deletion, Gene Expression Regulation, Neoplastic, Genetic Complementation Test, Glioblastoma, Humans, Hypoxia-Inducible Factor 1, Hypoxia-Inducible Factor 1, alpha Subunit, Insulin-Like Growth Factor I, Isoenzymes, Lymphokines, Membrane Proteins, Neoplasm Proteins, Nuclear Proteins, PTEN Phosphohydrolase, Phosphofructokinase-1, Phosphoric Monoester Hydrolases, Phosphotransferases (Alcohol Group Acceptor), Prostaglandin-Endoperoxide Synthases, Protein-Serine-Threonine Kinases, Proto-Oncogene Proteins, Proto-Oncogene Proteins c-akt, Recombinant Fusion Proteins, Transcription Factors, Transfection, Tumor Cells, Cultured, Tumor Suppressor Proteins, Vascular Endothelial Growth Factor A, Vascular Endothelial Growth Factors