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Fig. 9 | Journal of Hematology & Oncology

Fig. 9

From: Pharmacological targeting of the ephrin receptor kinase signalling by GLPG1790 in vitro and in vivo reverts oncophenotype, induces myogenic differentiation and radiosensitizes embryonal rhabdomyosarcoma cells

Fig. 9

GLPG1790 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 signals

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