Figure 1
From: Targeting RET–interleukin-6 crosstalk to impair metastatic dissemination in breast cancer
RET–IL-6 interaction mediates breast cancer cell motility. (A) GDNF binds to GFRα1 and induces RET activation. IL-6-mediated IL-6 receptor (IL6R) activation leads to co-receptor gp130 phosphorylation (P). (B) RET directly interacts with and activates FAK, while IL6R/gp130 activation induces JAK phosphorylation. Data presented by Gattelli and colleagues suggest a transient interaction between the IL6R:JAK and RET:FAK activated complexes that form in response to IL-6 and GDNF treatment, respectively [7]. (C) RET and FAK are essential to IL-6:JAK-mediated STAT3 activation underpinning the observed requirement for RET in IL-6-stimulated breast cancer cell migration and invasion.