Skip to main content
. 2018 Jul 17;13(2):125–135.

Figure 2.

The MAPK and related pathways in thyroid cancer.

Figure 2

Nuclear factor-κB (NF-κB) pathway that is leading to activation of the inhibitor of κB (IκB) kinase (IKK), resulting in the phosphorylation of IκB and dissociation from NF-κB. Free NF-κB then enters the nucleus to promote the expression of tumor-promoting genes. On the right side of the figure is the RASSF1–mammalian STE20-like protein kinase 1 (MST1)– fork head box O3 (FOXO3) pathway and activated MST1 then phosphorylates FOXO3 on Ser207. Phosphorylated FOXO3 enters the nucleus to promote the expression of pro-apoptotic genes in the FOXO pathway. In the middle of the figure is a unique and powerful mechanism of thyroid tumor genesis driven by BRAF-V600E. DAPK1, death-associated protein kinase 1; HIF1A, hypoxia-inducible factor 1α; MMP, matrix metalloproteinase; NIS, sodium–iodide symporter; TGFB1, transforming growth factor β1; TIMP3, tissue inhibitor of metallo proteinases 3; TPO, thyroid peroxidase; TSHR, thyroid-stimulating hormone receptor; TSP1, thrombospondin 1; UPA, urokinase plasminogen activator; UPAR, urokinase plasminogen activator receptor; VEGFA, vascular endothelial growth factor A (25).