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

Kisspeptins are peptides derived from the metastasis suppressor gene KISS1 interacting with GPR54 as their corresponding receptor. The KISS1/GPR54 system is one regulator of cellular motility mechanisms leading to decreased migration and 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 their endogenous 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 out with cells transfected with GPR54. All of the tested breast cancer cell lines expressed GPR54 in different amounts. No effects on proliferation were detected in the breast cancer cells expressing the receptor endogenously. In transfected neuronal cells overexpressing GPR54, proliferation was significantly inhibited by kisspeptin‑10. The results indicate that the antiproliferative action of kisspeptin depends on the nature of GPR54 expression. The effect was detected in an artificial system of cells transfected with GPR54 and not in cells expressing the receptor endogenously. Thus, the antiproliferative action of kisspeptin seems not to be important for pathophysiological processes.