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. 2014 Jan 28;16(1):301. doi: 10.1186/bcr3608

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Copyright © 2014 Isacke and Morandi; licensee BioMed Central Ltd.

The licensee has exclusive rights to distribute this article, in any medium, for 6 months following its publication. After this time, the article is available under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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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.