Signalling from Receptor Tyrosine Kinases under non-stimulated conditions and the impact on cancer aggressiveness (360G-Wellcome-105210_Z_14_Z)

Receptor Tyrosine Kinases (RTKs) relays signals which regulate processes such as cell growth, differentiation and cell division. Perturbations of signalling cascades can have serious consequences for the cell. It has previously been shown that proteins containing an SH3 domain can interact with a proline-rich region at the intracellular part of the RTK Fibroblast Growth Factor Receptor 2 (FGFR2), which consequently either inactivates the receptor or relays a downstream signal without any extracellular stimuli. Preliminary data suggests that FGFR2 and other RTK peptides containing the proline-rich motif can interact directly or indirectly with proteins containing SH3 domains. The aims of this project are to verify the interaction between FGFR2 and the proteins Fyn and LASP1, and also the interaction between the RTK ERBB2 (Epidermal Growth Factor family member) and Fyn, and possibly LASP1. Further investigation of the signalling pathways under non-stimulated conditions will be carried out, and their implications in cancer metastasis.