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Kisspeptin-10

KP-10, Metastin (45-54), Kisspeptin-10 (human), KiSS-1

Quick Stats
Studies 877
Trials 47
Score 1
2005 pubmed 128 citations

KiSS1 suppresses metastasis in human ovarian cancer via inhibition of protein kinase C alpha.

Jiang. Ying Y; Berk. Michael M; Singh. Lisam Shanjukumar LS; Tan. Haiyan H; Yin. Lihong L; Powell. C Thomas CT; Xu. Yan Y

Key Findings

  • KiSS1 reduces ovarian cancer cell migration and colony formation without affecting growth
  • In mice, KiSS1 expression cut metastatic spread by more than half
  • The anti‑metastatic effect is largely reversed when PKCα activity is restored

Practical Outcomes

  • For most biohackers, this research isn’t directly usable – it’s an early‑stage cancer study with no dosage, safety, or protocol information for humans. It simply points to KiSS1 as a potential future drug target, not a current supplement or lifestyle tweak.

Summary

The study shows that a protein called KiSS1 can slow down the spread of ovarian cancer cells in lab experiments and mice, mainly by blocking a specific enzyme (PKCα). However, it doesn’t give any guidance on how to use kisspeptin‑10 as a supplement or treatment for everyday health goals.

Abstract

Metastasis is a vital target for cancer treatment, since the majority of cancer patients die from metastatic, rather than the primary disease. KiSS1 has been identified as a metastasis suppressor gene in melanoma and breast carcinomas. We show here that KiSS1 is also a metastasis suppressor in human ovarian cancer. Overexpression of KiSS1 in ovarian cancer cells inhibits cell migration induced by serum or lysophosphatidic acid (LPA), and colonization in soft agar, but not cell proliferation, representing the characteristics of a metastasis suppressor gene. Furthermore, using an experimental metastatic mouse model, we show that expression of KiSS1 in SKOV3 ovarian cancer cells suppresses >50% metastatic colonization in mice (P < 0.0001). We find that activating protein kinase C (PKC) reverses about 80% of the inhibited cell migration induced by KiSS1, while down-regulation of PKCalpha with shRNA restores KiSS1 effect, providing evidence that inhibiting PKCalpha may be an important mechanism of the effect of KiSS1. These results suggest that KiSS1 is a metastasis suppressor of ovarian cancer and may be a potential molecular target for the treatment.

Study Information

Provider

pubmed

Year

2005

DOI

10.1007/s10585-005-8186-4

Citations

128

References

37