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Mechanisms of the Antiangiogenic Effects for Cancer by the Aspirin
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  • Bin Yang,
  • Shiyuan Xie,
  • youqiong wang,
  • Yixuan Huang
Bin Yang
Guangxi Medical University
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Shiyuan Xie
Guangxi Medical University
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youqiong wang
Guangxi Medical University
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Yixuan Huang
Guangxi Medical University
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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.