Kisspeptin-10 inhibits the migration of breast cancer cells by regulating epithelial-mesenchymal transition.

Abstract

Breast cancer is the leading cause of cancer-related death in women. Kisspeptin-10 (KP-10) is a shorter fragment of KISS1. In the present study, we demonstrated the antitumor effects of KP-10 on human breast cancer cell lines, MDA-MB-231 and MDA-MB-157, both in vitro and in vivo. KP-10 was observed to induce apoptosis and inhibit the mobility of MDA-MB-231 and MDA-MB-157 cells. Correspondingly, KP-10 suppressed tumor growth in established xenograft tumor models and improved the survival rate of tumor-bearing mice. The formation of intratumoral microvessels was inhibited following treatment with KP-10. Finally, we confirmed that KP-10 inhibited cell mobility via epithelial-mesenchymal transition (EMT). Overall, the present study demonstrated that KP-10 suppressed breast cancer and human umbilical vein endothelial cell (HUVEC) growth both in vivo and in vitro. KP-10 is a novel regulator of EMT in breast cancer cells. However, additional studies are needed to confirm these results in other cell types.

• Authors: Guo-Qing Song, Yi Zhao
• Journal: Oncology reports (Oncol Rep) Vol. 33 Issue 2 Pg. 669-74 (Feb 2015) ISSN: 1791-2431 [Electronic] Greece
• PMID: 25420482 (Publication Type: Journal Article)

Chemical References

• Antineoplastic Agents
• KISS1 protein, human
• Kisspeptins

Topics

• Animals
• Antineoplastic Agents (administration & dosage, pharmacology)
• Apoptosis
• Breast Neoplasms (blood supply, drug therapy, metabolism)
• Cell Line, Tumor
• Cell Movement (drug effects)
• Cell Proliferation
• Chick Embryo
• Epithelial-Mesenchymal Transition (drug effects)
• Female
• Gene Expression Regulation, Neoplastic
• Human Umbilical Vein Endothelial Cells
• Humans
• Kisspeptins (administration & dosage, pharmacology)
• Mice
• Neovascularization, Pathologic (drug therapy)
• Xenograft Model Antitumor Assays