2. Antiangiogenic mechanisms for the prevention and therapy of cancer by aspirin
In angiogenesis, the therapeutic concentration of aspirin can cause a significantly reduction in vessel tubule formation, while the high levels of endothelial cell apoptosis could triggered by aspirin at the higher concertration (Borthwick et al., 2009). Moreover, present studies show that aspirin significantly inhibits proliferation of normal human dermal microvascular endothelial cells (HuDMEC) and human umbilical vein endothelial cells (HUVEC) (Pearce et al., 2003; Boonmasawai et al., 2009). Furthermore, ASA also blocks endothelial cell migration after stimulation with VEGF (Navone et al., 2018), cancer cell (Maity et al., 2019) or ADP (Battinelli et al., 2011). However, the mechanism of these effects is complex. Many endogenous angiogenesis stimulators and inhibitors reside within the host microenvironment, including Interleukin-8 (IL-8), Fibroblast growth factor-1 (acidic FGF, FGF1), Fibroblast growth factor-2 (basic FGF, FGF2), Vascular endothelial growth factor (VEGF), vascular permeability factor (VPF) and Platelet-derived growth factor (PDGF) as well as others (Li et al., 2012). Aspirin could suppress angiogenesis and curb tumor growth by inducing these inhibitors and inhibiting these stimulants (FigureĀ 1).