Receptor tyrosine kinases (RTKs), epidermal growth factor receptor (EGFR), and its variant EGFRvIII activate the PI3K/AKT signaling pathway, subsequently influencing mTOR activity

Receptor tyrosine kinases (RTKs), epidermal growth factor receptor (EGFR), and its variant EGFRvIII activate the PI3K/AKT signaling pathway, subsequently influencing mTOR activity. Activation of RTKs, EGFR, and EGFRvIII leads to the phosphorylation and activation of PI3K, which converts PIP2 to PIP3 [18]. This conversion recruits and activates AKT, which in turn phosphorylates and activates mTOR. Activated mTOR functions as a major inhibitor of autophagy by phosphorylating and inhibiting key autophagy-initiating proteins, such as ULK1/2 [52]. This inhibition prevents the formation of autophagosomes and, subsequently, blocks the autophagic process, allowing for the accumulation of damaged proteins and organelles within the cell. mTOR pathway: Inhibition of autophagy occurs through the mTOR pathway, which is activated by abundant nutrients. Under conditions of nutrient deficiency, energy deficiency, and oxidative stress, mTOR is inhibited, leading to the induction of autophagy

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Importance of Autophagy Regulation in Glioblastoma with Temozolomide Resistance (2024) Young Keun Hwang, et al. Cells. 2024 Aug;13(16). Figure: F1. Homo sapiens

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