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The PI3K/AKT/mTOR pathway is an intracellular signaling pathway involved in numerous biological processes such as cell proliferation and apoptosis, angiogenesis, and glucose metabolism1,2. The pathway is initiated by the binding of extracellular growth factors to transmembrane receptor tyrosine kinases (RTKs) such as EGFR3,4, upon which phosphatidylinositol 3-kinase (PI3K) is activated and subsequently activates the serine/threonine protein kinase B (PKB/AKT). This leads to serine and/or threonine phosphorylation of a range of downstream substrates which often themselves are kinase/phosphatases or other signaling molecules which mediate the various cell biologies.
Dysregulation of this pathway has been associated with the development of a number of human diseases including, diabetes, autoimmunity, and cancer5. Enhanced activation can occur through several mechanisms, including inactivation of negative regulator phosphatase and tensin homolog (PTEN) and activating mutations, and gene amplification of the gene encoding PIK3CA6.
Agents that target the regulators in this pathway show attractive therapeutic potential, with multiple drugs targeting either single PI3K, AKT, or downstream effector mechanistic target of rapamycin (mTOR) or both PI3K and mTOR (dual inhibitors) already either commercialized or in development2,3,7.