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).