Mesoporous Silica Nanoparticles as an Antitumoral-Angiogenesis Strategy

Tumors depend heavily on angiogenesis for nutrient derivation and their subsequent metastasis. Targeting tumor induced angiogenesis per se can address both tumor growth and progression simultaneously. Here, we show that we could elegantly restrict the endothelial cells angiogenic behavior through digital size control of mesoporous silica nanoparticle (MSN). This antiangiogenesis effect was derived from the particle size dependent uptake and production of intracellular reactive oxygen species (ROS) that directly interfered with p53 tumor suppressor pathway. The resulting signaling cascade wrestled back the tumoral control of endothelial cells' migration, invasion, and proliferation. Overall, a mere control over the size of a highly oxidative reactive surfaced nanoparticle could provide an alternative strategy to curb the tumor induced angiogenesis process in a conventional drug-free manner.