Hsien-Ming Wu, Liang-Hsuan Chen, Wei-Jung Chiu, Chia-Lung Tsai

Kisspeptin Regulates Cell Invasion and Migration in Endometrial Cancer

  • Endocrinology, Diabetes and Metabolism
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Abstract Kisspeptin, product of KISS1 gene and its receptor play important roles in obstetrics, gynecology and cancer cell metastasis and behavior. In hypothalamic-pituitary-gonadal axis and placentation, Kisspeptin/Kisspeptin receptor affects hormone release and represses trophoblast invasion into maternal deciduae. Endometrial cancer is one of the common gynecological cancers and is usually accompanied by metastasis, the risk factor that causes death. Recently, researches demonstrate Kisspeptin/Kisspeptin receptor expression in aggressive stage endometrial cancer tissues. However, the detailed mechanism of Kisspeptin/Kisspeptin receptor in regulating the motility of endometrial cancers is not well understood. In this study, we use endometrial cancer cell lines RL95-2, Ishikawa, HEC-1-A and HEC-1-B as models to explore the molecular mechanism of Kisspeptin on cell motility. First, we discovered that Kisspeptin/Kisspeptin receptor was expressed in endometrial cancer cells, and Kisspeptin significantly regulated the migration and invasion of endometrial cancer cells. Furthermore, we explored the epithelial–mesenchymal transition (EMT) marker expression and the underlying signalings were regulated upon Kisspeptin treatment. In conclusion, we suggest that Kisspeptin regulates endometrial cancer cell motility via FAK and Src expression and the following ERK1/2, N-Cadherin, E-Cadherin, beta-Catenin, Twist, and MMPs signaling pathway. We expect the above molecules could be a candidate for the development of new approaches and therapeutic targets.

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