Figure 6.
Taking advantage of the differential oxidative stress response of cancer cells and endothelial cells (ECs). (A) A pro-angiogenic ferroptosis-like mechanism, through the generation of ROS, accumulation of lipid peroxides and glutathione (GSH) depletion, is implicated in the promotion of ECs hyperactivation, vessels leakiness and cancer cell adhesion and intravasation. (B) Propranolol (Prop) ROS scavenging activity is anti-angiogenic, impairing ECs activation underlined by the ferroptosis-like mechanism. (C) The combination of SeChry@PUREG4 nanoparticles and Prop was unraveled as a potential cancer therapy. SeChry@PUREG4 induces cancer cell death mediated by pro-oxidative features, while Prop stabilizes ECs and prevents the formation of a leakier vasculature, avoiding metastasis. Prop enhances the pro-oxidative features of Sechry@PUREG4 effect.