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. 2016 Jul 27;12(4):2567–2573. doi: 10.3892/ol.2016.4914

Figure 1.

Figure 1.

Schematic diagram of the IGF-1R downstream signaling cascades. IGF-1 acts as a ligand to IGF-1R. Autophosphorylation and recruitment of the adaptor proteins IRS-1, IRS-2 and Shc occurs. The interaction of IRS-1 and IRS-2 with IGF-1R induces the activation of PI3K. PI3K converts PIP2 to PIP3, which codes for the activation of AKT and consequently the dis-inhibition of mTOR oncoprotein. In parallel, Shc activation induces the activation of the RAS/RAF/MAPK pathway, which results in activation and phosphorylation of c-Myc transcription factor. Another signaling cascade downstream of IGF-1R is the JAK/STAT pathway, where direct activation of Jak kinases occurs, leading to the activation and phosphorylation of several STAT molecules. The most important of these, STAT3, acts as a transcription factor for numerous oncogenes. IGF-1, insulin-like growth factor 1; IGF-1R, IGF-1 receptor; IRS, insulin receptor substrate; PI3K, phosphatidylinositol 3-kinase; PIP2, phosphatidylinositol 4,5-bisphosphate; PIP3, phosphatidylinositol 3,4,5-trisphosphate; mTOR, mammalian target of rapamycin; MAPK, mitogen-activate protein kinase; JAK, Janus kinase; STAT, signal transducer and activator of transcription.