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Role of the Prostaglandin E₂ Receptor in Mammary Tumor Metastasis¹

University of Maryland Cancer Center and Department of Pathology, University of Maryland School of Medicine, Baltimore, Maryland 21201

Both clinical and experimental breast tumors often synthesize high levels of prostaglandins, most notably prostaglandin E₂ (PGE₂). We have reported previously that metastatic murine mammary tumor cells also express a high-affinity PGE₂ receptor. We have now shown that the receptor plays a functional role in the metastasis of two mammary tumor cell subpopulations, lines 66 and 4526. We showed that three agents, LEO101 (LEO Pharmaceuticals), SC19220 (Searle Co.), and AH6809 (Glaxo Co.), antagonize [³H]PGE₂ binding to these cells and block PGE₂-mediated elevation of intracellular cyclic AMP. Pretreatment of line 66 cells with nontoxic concentrations of any of the three receptor antagonists prior to i.v. injection results in more experimental lung colonies. As shown previously, and confirmed here, pretreatment of these cells with indomethacin (which inhibits endogenous PGE synthesis and therefore increases detectable PGE receptor) inhibits metastasis. Thus, the tumor cell PGE₂ receptor contributes to the ability of murine mammary tumor cells to metastasize.

¹ Supported by NIH Grant CA37943.

² To whom requests for reprints should be addressed, at Department of Pathology, University of Maryland School of Medicine, 10 South Pine Street, Baltimore, MD 21201.

Received 11/13/90. Accepted 2/ 1/91.

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