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Metastin, the final peptide of the KiSS-1 gene, has been proposed to suppress cell motility.
While all cell lines demonstrated hOT7T175 mRNA expressions, only Caki-1 had KiSS-1 transcripts.
This study was designed to evaluate the mechanism of how KiSS-1 works and to assess effects of a synthesized truncated KiSS-1 protein on the invasive ability of renal cell carcinoma (RCC) cells.
A synthesized truncated KiSS-1 peptide, metastin (45 54), produced a marked suppression of the invasive ability in KU19-20 cells, which were deficient for KiSS-1 transcripts, but not in Caki-1 cells.
Dual fluorescence labeling with a specific mouse monoclonal antibody against LHβ demonstrates that KiSS-1 and GPR54 are expressed by the gonadotrophs.
Although effects of a metastasis suppressor gene, KiSS-1, have been postulated to be mediated by its receptor, hOT7T175, the mechanism of such effects remains unknown.
Recent studies have demonstrated that the gonadotropin hypersecretion in postmenopausal women is secondary to increase of KiSS-1 mRNA from the hypothalamus neurons, which encoded kisspeptin peptides.
3 MSGs (CDH1, TIMP3 and KiSS-1) were significantly methylated.
The link between KiSS-1 and MED23 (CRSP3, DRIP130) has been described previously: MED23 is a cofactor required for expression of KiSS-1 [ 13].
Hammerhead ribozymes targeting Kiss-1 and Kiss-1R were designed using Zuker's mRNA Fold programme [ 14] based on the secondary structure of Kiss-1 and Kiss-1R mRNA.
