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Fig. 2 | Molecular Cancer

Fig. 2

From: IGF-IR signaling in epithelial to mesenchymal transition and targeting IGF-IR therapy: overview and new insights

Fig. 2

Basic molecular processes and signaling pathways contributing to the epithelial-mesenchymal transition (EMT). EMT is a developmental process by which epithelial cells lose their cell-cell adhesions and acquire mesenchymal cells identity. Loss of epithelial marker such as E-cadherin and the gain of mesenchymal marker such as Vimentin are considered as hallmarks in the initiation and execution of EMT. In many human tumors, the expression of multiple RTKs and their ligands induce autocrine growth factor loops. The activated RTKs induce signaling via PI3K/Akt and MAPK/ERK downstream signaling pathways, which up-regulates transcriptional factors (ZEB1/2 and Snail1/2) and causes EMT progression via binding to E-boxes of E-cadherin gene. TGF-β induces EMT through the activation of Smad2 signaling or other non-canonical signaling pathways (PI3K/Akt or MAPK/ERK pathways). Activation of NF-κB signaling can induce EMT program through up-regulating Twist1/2. In addition, activation of Notch, Wnt/β-catenin and Hedgehog signaling also contribute to the progression of EMT via regulation of Snail1/2

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