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. 2018 Jul 27;16(4):4095–4104. doi: 10.3892/ol.2018.9227

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Copyright: © West et al.

This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

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Figure 1. — STAT3 activation pathway. STAT3 is activated through the interaction of cytokines and growth factors. Growth factors have intrinsic kinase activity, whereas the receptors of ligands have associated JAK that, when phosphorylated, acts as a platform for un-phosphorylated STAT3 to become activated. Phosphorylated STAT3 dimers (not shown in figure for simplicity) translocates to the nucleus where it up-regulates a variety of genes that can contribute to tumourigenesis. The STAT3 pathway is negatively regulated by a number of ways. SOCS3 inhibits the phosphorylation of JAK proteins and PIAS3 inhibits dimerisation of STAT3 monomers. Phosphorylated STAT3 dimers are not shown for simplicity.