Antitumor effect of dipyridamole mediated by inhibiting the interaction between platelets and tumor cells

Figures

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  Fig. 1. Platelets are essential components in the tumor microenvironment. Platelets bind to and protect circulating tumor cells from hemodynamic forces and immune cells while they travel in the bloodstream. Platelets can assist circulating tumor cells in spreading to distant tissues via the bloodstream and promote angiogenesis associated with primary tumor cells

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  Fig. 2. The EMT process involves three steps: loss of cell–cell adhesion, loss of apical-basal polarity, become invasive mesenchymal cells. EMT generally results in decreased expression of epithelial genes, such as E-cadherin, claudin occludin, Zo-1, Muc1. EMT promotes increased expression of mesenchymal genes, for example, N-cadherin, Vimentin, fibronectin, FSP-1, Β-catenin

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  Fig. 3. After platelet activation, alpha granules release platelet-derived factors such as PDGF, TGF-β, and LPA. Platelet-related factors combine with corresponding receptors to promote EMT transcription program through different signal pathways

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  Fig. 4. PDGF, FGF and EGF can activate ERK signal through the Ras-Raf-MEK1/2-ERK signaling module. ERK dominates cell movement through phosphorylating FAK, MLCK, or calpain