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- W2617686875 endingPage "189" @default.
- W2617686875 startingPage "153" @default.
- W2617686875 abstract "The PI3K/AKT/mTOR pathway is frequently activated in various human cancers and has been considered a promising therapeutic target. Many of the positive regulators of the PI3K/AKT/mTOR axis, including the catalytic (p110α) and regulatory (p85α), of class IA PI3K, AKT, RHEB, mTOR, and eIF4E, possess oncogenic potentials, as demonstrated by transformation assays in vitro and by genetically engineered mouse models in vivo. Genetic evidences also indicate their roles in malignancies induced by activation of the upstream oncoproteins including receptor tyrosine kinases and RAS and those induced by the loss of the negative regulators of the PI3K/AKT/mTOR pathway such as PTEN, TSC1/2, LKB1, and PIPP. Possible mechanisms by which the PI3K/AKT/mTOR axis contributes to oncogenic transformation include stimulation of proliferation, survival, metabolic reprogramming, and invasion/metastasis, as well as suppression of autophagy and senescence. These phenotypic changes are mediated by eIF4E-induced translation of a subset of mRNAs and by other downstream effectors of mTORC1 including S6K, HIF-1α, PGC-1α, SREBP, and ULK1 complex." @default.
- W2617686875 created "2017-06-05" @default.
- W2617686875 creator A5050224620 @default.
- W2617686875 creator A5054898754 @default.
- W2617686875 date "2017-01-01" @default.
- W2617686875 modified "2023-10-18" @default.
- W2617686875 title "Oncogenic Roles of the PI3K/AKT/mTOR Axis" @default.
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