Proceedings of the 13th International Conference on Thrombosis and Hemostasis Issues in Cancer, 2026

Platelet-derived thromboxane A2 induces cyclooxygenase-2 and epithelial-mesenchymal transition marker genes in U-87MG human glioblastoma cells

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Published: 16 April 2026
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Glioblastoma (GBM) is an aggressive, treatment-resistant brain tumor. Elevated platelet counts are associated with tumor growth, and platelets accumulate in GBM tumors. Our study found that cyclooxygenase (COX)-2 expression and prostaglandin (PG)E₂ biosynthesis increase during the formation of U-87MG GBM cell spheroids. The COX-2 inhibitors celecoxib and rofecoxib inhibited PGE2 biosynthesis and reduced U-87MG spheroid growth. In cocultures of platelets with U-87MG spheroids, enhanced thromboxane (TX)B₂ was reduced by the selective exposure of platelets to aspirin, suggesting a platelet origin. In U-87MG cells, platelets increased the expression of COX-2 and epithelial-mesenchymal transition (EMT) marker genes. We prevented these effects by pretreating platelets with aspirin to inhibit TXA2 biosynthesis or with a TXA2 receptor antagonist. A TXA2 mimetic stimulated the expression of both COX-2 and epithelial-mesenchymal transition (EMT) markers in spheroids. Altogether, these findings indicate that platelet TXA2 induces COX-2 and promotes EMT in U-87MG cells. Aspirin, by inhibiting platelet TXA2, could contribute to reduced tumor growth and invasion in GBM.

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Citations

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Supporting Agencies

Ministero dell’Istruzione, dell’Università e della Ricerca (MIUR) , European Union (European Social Fund- PON Research and Innovation 2014-2020)

How to Cite



1.
Di Berardino S, Contursi A, Tacconelli S, Ahfaz HA, Patrignani P. Platelet-derived thromboxane A2 induces cyclooxygenase-2 and epithelial-mesenchymal transition marker genes in U-87MG human glioblastoma cells. Bleeding Thromb Vasc Biol [Internet]. 2026 Apr. 16 [cited 2026 Apr. 17];5(s1). Available from: https://www.btvb.org/btvb/article/view/443