Figure 1.

(A) Schematic of the structure of NSC@mSiO₂-SNO/ICG NPs and their passive accumulation in tumors via the EPR effect. (B) X-ray radiation on this system would trigger multiple tumoricidal responses by: (I) increasing dose deposition to accelerate radiolysis, (II) producing cytotoxic ROS by activating ICG based on the scintillation effect of NSC, and (III) releasing high levels of NO due to radiation fracture of S-N bonds. The above combined therapeutic processes would promote p53 up-regulation for apoptosis and DNA damage. The high NO levels would improve hypoxia and promote HIF1α down-regulation within the TME.