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The interactions of tumor cells with platelets contribute to the progression of tumor malignancy, and the expression levels of platelet aggregation‐inducing factors positively correlate with the metastatic potential of osteosarcoma cells. However, it is unclear how tumor‐platelet interaction contributes to the proliferation of osteosarcomas. We report here that osteosarcoma‐platelet interactions induce the release of platelet‐derived growth factor ( PDGF ) from platelets, which promotes the proliferation of osteosarcomas. Co‐culture of platelets with  MG 63 or  HOS  osteosarcoma cells, which could induce platelet aggregation, enhanced the proliferation of each cell line  in vitro . Analysis of phospho‐antibody arrays revealed that co‐culture of  MG 63 cells with platelets induced the phosphorylation of platelet derived growth factor receptor ( PDGFR ) and Akt. The addition of supernatants of osteosarcoma‐platelet reactants also increased the growth of  MG 63 and  HOS  cells as well as the level of phosphorylated‐ PDGFR  and ‐Akt. Sunitinib or  LY 294002, but not erlotinib, significantly inhibited the platelet‐induced proliferation of osteosarcoma cells, indicating that  PDGF  released from platelets plays an important role in the proliferation of osteosarcomas by activating the  PDGFR  and then Akt. Our results suggest that inhibitors that specifically target osteosarcoma‐platelet interactions may eradicate osteosarcomas.

Platelets promote osteosarcoma cell growth through activation of the platelet‐derived growth factor receptor‐Akt signaling axis