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Tumor‐cell‐induced platelet aggregation is a glycoprotein‐dependent and lipoxygenase‐associated process
Author(s) -
Bastida Eva,
Almirall Lourdes,
Ordinas Antonio
Publication year - 1987
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/ijc.2910390617
Subject(s) - platelet , chemistry , lipoxygenase , biochemistry , receptor , cell culture , cell , platelet membrane glycoprotein , platelet activation , microbiology and biotechnology , biology , immunology , enzyme , genetics
To characterize the platelet receptor sites and the platelet metabolic pathways involved in tumor‐cell‐induced platelet aggregation, we have used a homologous system consisting of human platelets and 2 tumor cell lines of human origin, which activate platelets through different mechanisms. Preincubation of platelets with an MAb against platelet glycoprotein I b partially blocked tumor‐cell‐induced platelet aggregation, and preincubation of platelets with an MAb against the glycoprotein complex GPII b III a , totally blocked the aggregation induced by the 2 tumor‐cell lines. No inhibitory effect was found when platelets were treated with PAF‐receptor antagonists or with specific peptides which block the platelet sites involved in bacterially induced platelet aggregation. Compounds which raised intra‐platelet cAMP levels inhibited tumor‐cell‐induced platelet aggregation in a dose‐related manner. Inhibition of cyclo‐oxygenase by aspirin which blocked TxB 2 formation by platelets did not inhibit platelet aggregation induced by tumor cells whereas the BW755 compound which inhibits cyclo‐ and lipoxygenase blocked platelet aggregation. These results demonstrate that tumor‐cell‐induced platelet aggregation is a glycoprotein‐dependent and a lipoxygenase‐associated phenomenon.