TGF-beta signaling in thyroid cells for epithelial-mesenchymal transition (Homo sapiens)

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This pathway is based on the Figure 7 of “Cadherin 6 Is a New RUNX2 Target in TGF-β Signalling Pathway”(see bibliography). TGF-B is a target gene in thyroid cells in the causation of cancer. When TGF-B is activated, the pathway can take 2 directions, through a SMAD pathway or a Non-Smad pathway. Through the SMAD pathway, SMAD separates into SMAD2/3, SMAD4, and involves phosphates into the nuclear signalling. Through the Non-SMAD pathway, the activation of MAPK and Pi3k causes the activation of ERK, AKT and phosphates, and then into the nuclear signalling. Within the nuclear signalling, EMT-TF has two responses, early and late. With the early response, EMT-TF signals to Id1 and RUNX2, and with the late response, EMT-TF signals to Snai1 and Snai2. Depending on the response also dictates the type of marker that will follow. If early, N-CAD,FN1,VIM,TNC, and CDH6 all cause the activation of the Mesenchymal markers. If late, E-CAD, and CDH16 cause the inhibition of the Epithelial Markers.