Fig. 9From: Pharmacological targeting of the ephrin receptor kinase signalling by GLPG1790 in vitro and in vivo reverts oncophenotype, induces myogenic differentiation and radiosensitizes embryonal rhabdomyosarcoma cellsGLPG1790 molecular working models. GLPG1790 inhibits EPH receptor activity and blocks both forward and revers Ephrin signals which, synergistically or individually, support (i) activation of AKT/mTOR and MEK/ERK signalling that support proliferation and cancer stem cell phenotype; (ii) inhibition of pro-apoptotic signal mediated by JNKs; (iii) pro-differentiating signal sustained by p38; (iv) activation of damaged DNA repair molecular mechanisms; (v) motility and invasion abilities by sustaining the SRC-mediated integrin signalsBack to article page