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Kisspeptin-10

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

Quick Stats
Studies 877
Trials 47
Score 1
2008 pubmed 47 citations

Metastin inhibits migration and invasion of renal cell carcinoma with overexpression of metastin receptor.

Shoji. Sunao S; Tang. Xian Yan XY; Umemura. Shinobu S; Itoh. Johbu J; Takekoshi. Susumu S; Shima. Masanori M; Usui. Yukio Y; Nagata. Yoshihiro Y; Uchida. Toyoaki T; Osamura. Robert Yoshiyuki RY; Terachi. Toshiro T

Key Findings

  • Kidney tumor samples show high levels of the metastin receptor (hOT7T175).
  • Metastin (10 µM) blocks migration and invasion of RCC cell lines Caki‑1 and ACHN in vitro.
  • Metastin does not affect proliferation of these cancer cells.
  • The anti‑migration effect is linked to Rho‑kinase signaling and can be reversed by a Rho‑kinase inhibitor.

Practical Outcomes

  • At this stage there’s no direct way to use metastin for health or anti‑cancer purposes outside the lab. The study is early‑stage and only shows cell‑culture effects, so biohackers should not try dosing protocols until human safety and efficacy are established.

Summary

Researchers found that kidney cancer cells have a lot of the receptor for a peptide called metastin, and when they added metastin in the lab it stopped the cancer cells from moving and invading, but it didn’t slow their growth. This effect involved changes in cell structures that were blocked by a Rho‑kinase inhibitor.

Abstract

Metastin, the final peptide of the KiSS-1 gene, has been proposed to suppress cell motility. This study investigated whether renal cell carcinoma (RCC) tissue expresses metastin or its receptor, and clarified whether metastin can suppress migration and/or invasion and/or proliferation of RCC cells in vitro. Twenty-five RCC samples were submitted. Fresh RCC tissues were prepared for real-time RT-PCR, and formalin-fixed and paraffin-embedded tissues blocks were examined by immunohistochemistry. RCC cell lines Caki-1 and ACHN were supplied for cell migration, invasion, and proliferation assays. Real-time RT-PCR was performed by using Taq Man gene expression system. ENVISION system was used in immunohistochemistry. Wound-healing assay and matrigel assays were used to identify migration and invasion abilities of RCC cell lines. Cell Counting Kit-8 was applied to measure the cell proliferation. Cell morphology was examined under a META system. Statistical analysis was performed with SPSS15.0J. In twenty-five RCC samples, the mRNA level of metastin receptor was identified to be significantly higher than non-neoplastic renal cortex by real-time RT-PCR (p=0.011). Immunohistochemical study also detected metastin receptor protein in all RCC tumors. In vitro, this study showed that metastin inhibited migration and invasion of Caki-1 and ACHN cells. In contrast, it had no effects on cell proliferation. Metastin (10 micromol/l) induced excessive formation of focal adhesions and stress fibers in Caki-1 and ACHN cells; this phenomenon was inhibited by pretreating pharmacological Rho-kinase inhibitor (Y-27632) to those cells. This is the first report regarding overexpression of the metastin receptor hOT7T175 in human RCC. We demonstrate that metastin can inhibit migration and invasion of the RCC cell line, which is regulated by a Rho-kinase inhibitor. Metastin and its receptor are therefore probable targets for suppressing RCC.

Study Information

Provider

pubmed

Year

2008

Date

2008-03-11T00:00:00.000Z

DOI

10.1016/j.eururo.2008.02.048

Citations

47

References

27