AKT1 and glioblastoma: For instance, it has been observed that the ectopic overexpression of wild-type PTEN in the human U373 glioblastoma-derived cell line lacking functional PTEN reduced IGF-1- and hypoxia-induced Akt activation and consequently the HIF-1α stabilization and expression of its target gene products, including glycolytic enzymes, PGK-1 and PFK, COX-1 and VEGF [41].