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Effect of different platelet agonists on intracellular free CA ++ concentrations in human tumor cells: Possible role in tumor growth
Author(s) -
Saporiti Anna,
Brocchieri Alessandra,
Porta Camillo,
Moroni Mauro,
Grignani Guido
Publication year - 1995
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.2910620310
Subject(s) - cell culture , hela , in vitro , chemistry , thrombin , cancer research , microbiology and biotechnology , platelet , biology , immunology , biochemistry , genetics
Modulation of cytoplasmic Ca ++ concentration is a mechanism common to signal transduction pathways regulating many cellular phenomena, including the interactions of tumors with the hemostatic system. We have investigated the pro‐aggregating and pro‐coagulant activities of human tumor cell lines cultured in vitro and the ability of different platelet agonists to induce Ca ++ transients in these cells. Cells of a malignant mesothelioma line activated platelets by a thrombin‐dependent mechanism; on the contrary, HeLa cells, derived from a uterine cervical cancer, possessed ADP‐dependent pro‐aggregating activity, and DND‐1A melanoma cells did not stimulate platelet aggregation. All cell lines showed a tissue‐factor‐like procoagulant property, more pronounced in mesothelioma cells. Furthermore, ADP was able to induce a transient increase in cytoplasmic Ca ++ concentration in tumor cells from all lines; collagen showed this effect in mesothelioma cells and in HeLa cells, and thrombin was effective only in mesothelioma cells. PAF never induced Ca ++ fluxes in any of the cell lines investigated. Finally, the calcium‐channel blocker verapamil inhibited agonist‐induced Ca ++ transients in tumor cells and in vitro tumor‐cell growth. These data may help to identify new possible mechanisms of the 2‐way interaction of tumors with the hemostatic system. © 1995 Wiley‐Liss Inc.