Premium
Protracted treatment with phorbol ester modulates j‐7 human hepatoma‐cell‐induced aggregation and coagulation of human platelet‐rich plasma
Author(s) -
Ko Feng N.,
Yu Sheu M.,
Teng Che M.
Publication year - 1994
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.2910590520
Subject(s) - fibronectin , apyrase , vitronectin , coagulation , chemistry , medicine , endocrinology , platelet , fibrinogen , biochemistry , extracellular matrix
In heparinized human platelet‐rich plasma (PRP), J‐7 human hepatoma cells initially induced platelet aggregation; then a clot formed. ADP‐scavenger systems, apyrase and creatine phosphate/creatine phosphokinase did not inhibit this tumor‐cell‐induced platelet aggregation (TCIPA), whereas hirudin and concanavalin A completely blocked it. J‐7 cells also shortened the recalcification time of normal and of Factor‐VIII‐ and ‐IX‐deficient human plasma, although it was inactive in shortening the recalcification time of Factor‐VII‐deficient plasma. After treatment with phorbol 12,13‐dibutyrate (PDBu) for 5 to 90 min, the aggregation and coagulation abilities of J‐7 cells were unaffected. Prolonged treatment of J‐7 cells with PDBu but not with α‐PDBu for 24 and 72 hr resulted in gradual loss of aggregation and coagulation. Staurosporine antagonized the effect of PDBu and restored aggregation and coagulation in J‐7 cells. Protracted treatment with PDBu (24 or 72 hr) did not affect adherence of J‐7 cells to the extracellular‐matrix proteins ( i.e. , fibrinogen, fibronectin, laminin, vitronectin and collagen types I and IV) or to the surface of plastic culture dishes. The treatment also did not affect J‐7 cell detachment from plastic culture dishes. These in vitro results demonstrate that protracted phorbol ester treatment diminishes TCIPA and blood coagulation of tumor cells.