The PI3K–AKT network at the interface of oncogenic signalling and cancer metabolism

By Gerta Hoxhaj, B. Manning. Nature Reviews. Cancer, 2019

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Targeting PI3K/Akt signal transduction for cancer therapy (2021, background): “The phosphorylation of metabolic enzymes causes acute changes in the activities of metabolic pathways and the directionality of metabolic fluxes, while long-term changes in cellular metabolism are usually achieved by controlling gene expression programs.(147) Akt not only directly phosphorylates a v”
PI3K/Akt/mTOR Pathway and Its Role in Cancer Therapeutics: Are We Making Headway? (2022, background): “The PI3K/AKT/mTOR pathway is crucial for cell motility, growth, survival, and metabolism in cancer (14, 15).”
Oncogenic activation of PI3K-AKT-mTOR signaling suppresses ferroptosis via SREBP-mediated lipogenesis (2020, background): “Cancer cells usually endure elevated oxidative stress due to increased metabolic and proliferative burden (42, 43).”
Revisiting the Warburg effect: historical dogma versus current understanding (2020, background): “The key enzyme facilitating the entry at the branching point into the oxidative PPP is glucose-6-phosphate dehydrogenase (e.g. activated by phosphoinositide 3-kinase (PI3K), Akt–mechanistic target of rapamycin (mTOR), cMyc, mutant p53; Jiang et al. 2011; Hoxhaj & Manning, 2020).”