Inhibition of tumor cell induced platelet aggregation by prostacyclin and carbacyclin: an ultrastructural study.
Prostacyclin and its synthetic analog carbacyclin were compared as to their abilities to inhibit tumor cell-platelet interactions. Aggregation of rat platelets was induced in vitro by homologous rat Walker 256 carcinosarcoma cells. The extent of cellular interactions was examined ultrastructurally. The ultrastructural data presented here indicate that the tumor cell-platelet interactions began with individual platelets which initiated platelet chain formation in focal association with tumor cell surfaces. By mid-phase aggregation large homotypic platelet aggregates had formed with tumor cells positioned on the external surfaces of the emboli. Tumor cell-platelet interactions became progressively more extensive as tumor cells became enmeshed with growing platelet aggregates. Prostacyclin and carbacyclin inhibited tumor cell platelet interactions in a dose-dependent manner. Carbacyclin inhibition of tumor cell induced platelet aggregation was longer in duration but carbacyclin was 10-fold less effective than was prostacyclin. We report here that prostacyclin and carbacyclin inhibit both aggregation and the ultrastructural changes associated with tumor cell-platelet interactions.
Menter
D G
DG
Harkins
C
C
Onoda
J
J
Riorden
W
W
Sloane
B F
BF
Taylor
J D
JD
Honn
K V
KV
D000818:Animals; D002279:Carcinoma 256, Walker / Q000648:ultrastructure*; D002450:Cell Communication; D011464:Epoprostenol / Q000494:pharmacology* / Q000031:analogs & derivatives; D008854:Microscopy, Electron; D008855:Microscopy, Electron, Scanning; D010974:Platelet Aggregation / Q000187:drug effects*; D051381:Rats; D011919:Rats, Inbred Strains
C026678:carboprostacyclin; D011464:Epoprostenol