Mechanisms of the Antiangiogenic Effects for Cancer by the Aspirin
- Bin Yang,
- Shiyuan Xie,
- youqiong wang,
- Yixuan Huang
Abstract
Aspirin as an old drug extracted from willow bark and widely used in the
prevention and treatment of cardiovascular diseases. Increasing evidence
have shown that aspirin use may significantly reduce the angiogenesis of
cancer, while the mechanism of the association between angiogenesis and
aspirin is complex. Although COX-1 is widely known as a target of
aspirin, several studies reveal other antiangiogenic targets of aspirin,
such as angiotensin II, Glucose transporter 1, heparanase, and matrix
metalloproteinase. In addition, some evidence indicates that aspirin may
produce antiangiogenic effects after acting in different cell types,
such as endothelial cell, platelet, pericyte, and macrophage. In this
review, we concentrate on recent researches on the antiangiogenic
effects of aspirin in cancer, and analyze the molecular mechanisms of
aspirin and its metabolites. Moreover, we discuss some mechanisms
through which aspirin treatment may normalise existing blood vessels,
including preventing disintegration of endothelial adheren junctions and
recruiting pericytes. We also address the antiangiogenic effects and the
underlying mechanisms of aspirin derivatives, which aim to improve
safety and efficacy.