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ShareFeb. 22, 2007 — A new study finds that the secretion of a protein known as KISS1 reduces metastasis of cells that express it to multiple organs in mice, but the mechanism for this continues to elude researchers. The study appears in the Feb. 21 issue of the Journal of the National Cancer Institute.
The KISS1 protein also plays a role in sexual maturation when it is secreted and then processed into smaller peptides called kisspeptins, which in turn bind to a receptor known as GPR54. Kevin Nash, Ph.D., in the laboratory of Danny R. Welch, Ph.D., of the University of Alabama at Birmingham, and their colleagues wondered if the GPR54 receptor was also involved in metastasis suppression.
Using a human melanoma cell line that could not express KISS1, the researchers inserted one of two forms of the KISS1 gene into the cells—coding for either an unaltered form of KISS1 or a version that could not be secreted. The cells were later injected into mice that were monitored for changes in survival rates and metastatic activity of the injected cells.
The researchers concluded that KISS1 secretion was required for metastasis suppression of the melanoma cells. Only the cells with the intact form of KISS1 secreted kisspeptins, and these cells showed less metastatic activity when they were injected into the mice than those with the altered version. Mice that were injected with the gene for the intact KISS1 protein lived much longer, on average, than the mice with the non-secretable KISS1 cells. Furthermore, KISS1 blocked the growth of tumor cells that have already spread other organs. But, the authors conclude, the GPR54 receptors did not likely play a role in this process.
“The finding that KISS1 can inhibit metastatic growth in multiple organs is a particularly important feature for an antimetastatic molecular agent,” the authors write. “Finally, the finding that KISS1 can suppress metastasis in the apparent absence of GPR54 in tumor cells opens up the possibility that additional KISS1 metastasis suppressor receptors and signaling pathways exist with the potential to be selectively targeted.”
Note: The Journal of the National Cancer Institute is published by Oxford University Press and is not affiliated with the National Cancer Institute. Visit the Journal online at http://jnci.oxfordjournals.org/.
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