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Kisspeptins are peptides derived from the metastasis suppressor gene KISS1interacting with GPR54 as their corresponding receptor. The KISS1/GPR54 systemis one regulator of cellular motility mechanisms leading to decreased migrationand invasion. Its role in cell proliferation processes is not clearly understood.In this study, breast cancer cell lines, T47D, ZR75-1, MDA‑MB‑231, MDA‑MB‑435s,MDA‑MB‑453, HCC 70, HCC 1806, HCC 1937 and MCF‑7, were investigated for theirendogenous GPR54 expression by immunocytochemistry, RT‑PCR and western blot analysis.The effect of kisspeptin‑10 on proliferation was measured in MDA‑MB‑231, MDA‑MB‑435s,HCC 1806 and MCF‑7 cells. Further experiments on proliferation were carried outwith cells transfected with GPR54. All of the tested breast cancer cell linesexpressed GPR54 in different amounts. No effects on proliferation were detectedin the breast cancer cells expressing the receptor endogenously. In transfectedneuronal cells overexpressing GPR54, proliferation was significantly inhibitedby kisspeptin‑10. The results indicate that the antiproliferative action of kisspeptindepends on the nature of GPR54 expression. The effect was detected in an artificialsystem of cells transfected with GPR54 and not in cells expressing the receptorendogenously. Thus, the antiproliferative action of kisspeptin seems not to beimportant for pathophysiological processes.

Antiproliferative effects of kisspeptin-10 depend on artificial GPR54 (KISS1R) expression levels