Abstract
Metastasis is a complex multistep process that involves the impairment of cell-cell adhesion in the neoplastic epithelium, invasion into adjacent tissues and the dissemination of cancer cells through the lymphatic and haematogenous routes. The inhibition of the metastatic process at an early stage has become a hot topic in cancer research. The Kiss-1 gene, initially described as a suppressor of metastasis in malignant melanoma, encodes the Kiss-1 protein which can be processed to other peptides, e.g., Kisspeptin-10, Kisspeptin-13, Kisspeptin-14 and Kisspeptin-54. These peptides are endogenous ligands of the Kiss‑1 receptor (Kiss-1R), a G protein-coupled receptor (GPR) also known as hOT7T175, AXOR12 or GPR54. The Kiss-1 gene has been suggested as a suppressor of metastasis in a various types of cancer, including gastric cancer, oesophageal carcinoma, pancreatic, ovarian, bladder and prostate cancer, through the regulation of cellular migration and invasion. In the current review, we summarise the current understanding of the role of Kiss‑1 and Kiss‑1R in cancer and cancer metastasis.
Highlights
Metastasis is a complex multistep process that involves the impairment of cell-cell adhesion in the neoplastic epithelium, invasion into adjacent tissues and the dissemination of cancer cells through the lymphatic and haematogenous routes
It remains controversial to some degree, Kiss‐1 has been demonstrated as a suppressor of metastasis in the majority of cancers, including gastric cancer, oesophageal carcinoma, pancreatic, ovarian, bladder and prostate cancer
A possible explanation for the role played by Kiss‐1 in cancer biology can be extrapolated from the correlation between Kiss‐1 and Matrix metalloproteinases (MMPs), MMP‐9 and MMP‐2, whose significance in tumour invasion and metastasis formation is
Summary
Based on the study of subcutaneous xenografts established by inoculating Ishikawa cells into female nude mice, they reported that the decreased number of lymph node metastases of Kiss‐1R + Ishikawa cells was observed in metastin‐10‐treated mice, while there was no significant difference in the tumour size between the metastin treated and non‐treated groups. This indicates that Kiss‐1 affects the metastatic potential of cancer cells rather than directly inhibiting tumour growth [55].
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