Skip to main content
. 2020 Oct 2;10:572904. doi: 10.3389/fonc.2020.572904

Figure 1.

Figure 1

Scheme of the phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) pathway in the regulation of autophagy process. The PI3K/AKT/mTOR signaling pathway is activated by various receptor tyrosine kinases (RTKs), such as epidermal growth factor receptor (EGFR), vascular endothelial growth factor receptor (VEGFR), and platelet-derived growth factor receptor (PDGFR), while the pathway is negatively regulated by phosphatase and tensin homolog (PTEN). Hyperactivation of the PI3K/AKT/mTOR pathway inhibits autophagy, and suppression of the PI3K/AKT/mTOR pathway induces autophagy. mTOR complex I (mTORC1) plays a key role in the regulation of autophagy process. Under conditions of nutrient sufficiency, mTORC1 is activated and inhibits autophagy. Under starvation or low energy, AMP-activated protein kinase (AMPK) is activated and mTORC1 is inactivated, leading to the initiation of autophagy. Induction of autophagy can be summarized into several phases: initiation, nucleation, elongation, maturation, fusion, and degradation. Autophagy has a dual role in pro-survival or pro-cell death in GB progression. NF1, neurofibromin 1; PIP2, phosphatidylinositol-4,5-bisphosphate; PIP3, phosphatidylinositol-3,4,5-trisphosphate; PDK1, 3-phosphoinositide-dependent kinase-1; TSC1/2, tuberous sclerosis complex 1/2; RHEB, Ras homolog enriched in brain; LKB1, liver kinase B1; p70S6K, 70-kDa ribosomal protein S6 kinase; EIF4EBP1, eukaryotic translation initiation factor 4E-binding protein 1.