PI3K, composed of one catalytic (p110) domain and one regulatory (p85), can be activated by G-protein coupled receptor, RTK, IGF-R, and B-cell. Here we report a comprehensive PI3K/AKT/mTOR network that represents the intricate crosstalk between compensatory pathways, which can be utilized to study the AKT signalling mechanism in detail and improve the personalized combinatorial therapeutic strategies. The activation process of PI3K/AKT signaling pathway. Limited clinical success of the available targeted therapeutic agents and challenges mediated by tumour heterogeneity across different cancer types emphasize the importance of alterations in the PI3K/AKT/mTOR pathway in the design of effective personalized treatment strategies. The PI3K/AKT/mTOR pathway is regulated by a wide-range of upstream signalling proteins and it regulates many downstream effectors by collaborating with various compensatory signalling pathways, primarily with RAF/MEK/ERK pathway. There are several factors that ultimately result in resistance to PI3K inhibitors including (1) inactivation or loss of PTEN activity, (2) mutations and amplification of PI3K, (3) drug-related toxicities, (4) feedback upregulation leading to compensatory. PI3K signaling is deregulated in a variety of cancers. The phosphatidylinositol 3-kinase (PI3K)/AKT/mammalian target of the rapamycin (mTOR) signalling pathway is hyperactivated or altered in many cancer types and regulates a broad range of cellular processes including survival, proliferation, growth, metabolism, angiogenesis and metastasis. Signaling Molecules and Factors Contributing to PI3K Inhibitor Resistance.
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