Prostaglandin D2 formation by malignant melanoma cells correlates inversely with cellular metastatic potential.

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Abstract
B16 [mouse] malignant melanoma cell lines transform arachidonic acid and its transient metabolite, prostaglandin endoperoxide H2, into prostaglandin D2. The highly metastatic line, B16 F10, forms less prostaglandin D2 compared to the moderately metastatic parent line, B16 F1. Since platelet aggregation may be 1 factor involved in B16 metastasis and since prostaglandin D2 inhibits platelet aggregation, this prostaglandin could affect the outcome of platelet-tumor interactions, which may contribute ultimately to metastasis. Arachidonic acid metabolism may be another of the intrinsic biochemical properties of tumor cells that affects their metastasis. Quantitative release of unusual prostaglandins must be considered in this context.