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. 2011 Nov 5;2(11):833–849. doi: 10.18632/oncotarget.346

Figure 1. The PI3K pathway is central to proliferation, migration, and invasion in GBM cells.

Figure 1

Upon activation at the plasma membrane, the catalytic subunit of class IA PI3Ks phosphorylates phosphatidylinositol 4,5-bisphosphate (PIP2), converting it to phosphatidylinositol 3,4,5-triphosphate (PIP3). This results in the activation of several downstream pathways, including the Akt and mTOR pathways, which leads to increased proliferation and survival. PTEN activity converts PIP3 to PIP2. Interestingly, the p85α regulatory subunit has been shown to bind PTEN directly and enhance its lipid phosphatase activity [62]. This subunit may also be involved in the activation of migration and invasion-promoting pathways, possibly through the activation of small GTPases such as Cdc42 and Rac [23, 63]. p85α may interact with caspase 8 (in a non-apoptotic function of this caspase) to increase cell motility and Rac activation [55]. p85α has also been shown to interact with FAK, and this interaction correlates with FAK activation [14].