Relation of the IGF/IGF1R system to autophagy in colitis and colorectal cancer

Figure 3 Proposed model for the bi-directional IGF1R signaling-dependent modulation of the autophagic pathway. IGF1R targeting via suppression of the "canonical" PI3K/Akt/mTORC1 pathway stimulates the autophagy process. However, it can also result in a reduced formation of autophagosomal precursors at the plasma membrane. IGF1R depletion inhibits mTORC2, which reduces the activity of protein kinase C alpha and beta. This finally negatively impacts autophagosome precursor formation. IGF1R: Insulin-like growth factor receptor 1; PI3K: Phosphatidylinositol-3-kinase; AKT: Serine/threonine kinase, named protein kinase B (PKB); mTORC1/2: Mammalian target of rapamycin complex 1/2; PKC: Protein kinase C; ATG16L1: Autophagy-related protein 16-1.