Connections between insulin/insulin-like growth factor 1 signaling and metabolic pathways in tumor cells. Connections between insulin/insulin-like growth.

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Connections between insulin/insulin-like growth factor 1 signaling and metabolic pathways in tumor cells. Connections between insulin/insulin-like growth factor 1 signaling and metabolic pathways in tumor cells. Insulin receptor (IR) and IGF1R can either homo- or heterodimerize to activate their TK domains; this stimulates downstream RAS/RAF/MEK/ERK and RAS/PI3K/AKT/mTOR signal transduction pathways, which induce survival, proliferation, angiogenesis, and ribosomal synthesis of several proteins, including HIF1α. PI3K, RAS, and HIF1α promote crucial metabolic modifications in neoplastic cells, including glucose uptake and aerobic glycolysis, as well as de novo synthesis of fatty acids. Because RAS/RAF/MEK/ERK and RAS/PI3K/AKT/mTOR cascades can also be activated by other membrane receptors, including EGFR and HER2, combining inhibition of the IGF1/IGF1R pathway with targeting of other TK receptors or their downstream mediators (e.g., mTOR) could synergistically inhibit cancer cell proliferation and survival. EGFR, epidermal growth factor receptor; HER2, human epidermal growth factor receptor 2; HIF1α, hypoxia-inducible factor-1α; IGF1, insulin-like growth factor 1; IGFBP, IGF1 binding protein; IGF1R, IGF1 receptor; IR, insulin receptor; mTOR, mammalian target of rapamycin; PI3K, phosphoinositide 3-kinase; S6K, S6 kinase. Claudio Vernieri et al. Cancer Discov 2016;6:1315-1333 ©2016 by American Association for Cancer Research