Prostaglandin D₂ controls pulmonary metastasis of malignant melanoma cells

Abstract

Selective metastasis of malignant cells in various neoplastic processes is poorly understood. Metastasis seems to be associated with inherent biochemical and biological properties of tumour cells which guarantee their survival and multiplication. These properties may include surface enzymes¹, interaction with various host defence systems and cells^2–4, combination with host platelets⁵, or with the host endothelial cells, and adhesiveness of the metastatic cell. Fidler^2,6,7 has developed a series of malignant melanoma cells that are useful for studying tumour metastasis. By comparing the moderate metastatic parent line, B16F₁ to the highly metastatic Une, B16F₁₀, it is possible to study metastasis selectively. Prostaglandins influence various cell functions, and may be involved in regulation of neoplastic processes^8–10. We have recently reported that prostaglandin D₂ (PGD₂) formation by malignant melanoma cells in vitro is inversely correlated with their metastatic potential¹¹. The studies we describe here were designed to determine whether treating the cells with a cyclooxygenase inhibitor, which would block conversion of arachidonic acid to prostaglandins, would affect the metastatic rate of either cell. The results suggest that PGD₂ is involved in the metastasis of these cells.