Dipyridamole inhibits tumor progression by blocking platelet aggregation and platelet-mediated epithelial-to-mesenchymal transition via targeting the ERK-MAPK signaling pathway.
Does dipyridamole exert antitumor effects by inhibiting platelet-tumor cell interactions?
This review highlights the potential of the antithrombotic drug dipyridamole as a novel anticancer therapy by targeting platelet-tumor cell interactions.
Dipyridamole is a well-known antithrombotic and a vasodilator. It is used to treat cerebrovascular and cardiovascular diseases owing to its antiplatelet effects. Platelets play a key role in thrombosis and hemostasis, and after cancer cells enter the bloodstream, they interact with these cells to protect them and promote metastasis. Dipyridamole inhibits tumor progression by blocking platelet aggregation and platelet-mediated Epithelial-to-mesenchymal transition (EMT) via targeting the extracellular signal-regulated kinase (ERK)-mitogen-activated protein kinases (MAPK) signaling pathway, further highlighting its potential antitumor properties. However, studies on the anti-tumor mechanisms of dipyridamole are currently limited and incomplete. In this review, we summarize the pathways through which dipyridamole disrupts platelet-tumor cell interactions and exerts antitumor effects, aiming to inform the development of novel anticancer therapies.
Xue et al. (Fri,) conducted a review in Cancer. Dipyridamole was evaluated. Dipyridamole inhibits tumor progression by blocking platelet aggregation and platelet-mediated epithelial-to-mesenchymal transition via targeting the ERK-MAPK signaling pathway.