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Various studies support the view that analogs of luteinizing hormone-releasing hormone (LH-RH) exert some direct effects on mammary tumor cells. Recently, new LH-RH antagonists [Ac-D-Nal(2)1,D-Phe(pCl)2,D-Trp3,D-Hci6,D-Ala10]-LH-RH (SB-29) and [Ac-D-Nal(2)1,D-Phe(pCl)2,D-Trp3,D-Cit6,D-Ala10]LH-RH (SB-30), which are devoid of edematogenic effects, were synthesized. In this study, we examined whether these LH-RH antagonists inhibit the proliferation of MDA-MB-231 human mammary tumor cells in culture. [3H]Thymidine incorporation into DNA and cell number were measured. The antagonists induced up to 40% inhibition of [3H]thymidine incorporation in MDA-MB-231 cells. This inhibition was dose-dependent in the 0.3-30 microM range and could be demonstrated after 2 days of incubation in the presence of the peptides. An older antagonist, [Ac-D-Phe(pCl)1,2,D-Trp3,D-Arg6,D-Ala10]-LH-RH (ORG 30276), had a lesser effect, and the agonist des-Gly10-[D-Ser(tBu)6]LH-RH ethylamide (buserelin) had no effect. The antagonists SB-29 and SB-30 also inhibited the rate of cell growth, as measured by cell number, while the LH-RH agonist buserelin had no significant effect. These results support the concept that these new LH-RH antagonists can directly inhibit the growth of human mammary tumors and thus might be suitable for the treatment of breast cancer.

Inhibition of growth of human mammary tumor cells by potent antagonists of luteinizing hormone-releasing hormone.