Kisspeptin 10 Inhibited the Proliferation, Migration, and Stemness of Esophageal Cancer Cells via Regulating the SIX1/Wnt/β-Catetin Signaling.

Guo C, Wu G, Liu T

Journal of biochemical and molecular toxicology1 Apr 2025

PMID40192612DOI10.1002/jbt.70244PepBankPUB-40192612

Publisher page PubMedAsk about this study

Summary

The text of this summary is not shown here, because the article license does not allow reuse. Read it at the source (opens in a new tab)

Text rights: Publisher copyright. Results still quote short attributed sentences.

Results from this study7

No result from this study comes from a test of the peptide.

Natural levels measured1

These results measure the body's own peptide. Nobody was given the peptide. They are not evidence about taking it. They are left out of key results, evidence counts and charts.

01LabEndogenous levelEx vivo tissueOther
Expression of both KP-10 and GPR54 was significantly lower in esophageal cancer samples and cell lines than in healthy tissues.
In plain wordsThe body's own kisspeptin‑10 and its receptor were lower in esophageal cancer samples and cells than in healthy tissue.
Peptide
Kisspeptin-10
Outcome
DecreaseKP-10 and GPR54 expression in esophageal cancer
Study
n: not reported in source
Esophageal carcinoma tissues and cell lines
Comparator
Healthy tissues
Outcome group
Tumor growth · Cancer
Source sentences
Summary
Our results demonstrated significantly reduced expression of both KP-10 and GPR54 in EC samples and cell lines compared to healthy tissues.
1 context sentence(design, population, supporting numbers)
Summary · context
We first assessed KP-10 expression in esophageal carcinoma tissues and cell lines using immunohistochemistry, real-time PCR, and western blot analysis.
This result measures the body's own Kisspeptin-10. Nobody was given the peptide. It is not evidence about taking it.
Report a problemFND-4019261201

Studies that did not test the peptide alone6

In this study, Kisspeptin-10 was a lab tool or a carrier, part of a mix, or the subject of a lab method. These results are not evidence about taking Kisspeptin-10.

02LabNot a test of Kisspeptin-10 aloneIn vitro (cells)Efficacy outcome
In KYSE150 esophageal cancer cells, KP-10 overexpression inhibited cell growth.
In plain wordsIn esophageal cancer cells in the lab, raising KP-10 production slowed cell growth.
Peptide
Kisspeptin-10
Outcome
DecreaseCell growth after KP-10 overexpression
Study
n: not reported in source
KYSE150 esophageal cancer cells
Outcome group
Tumor growth · Cancer
Source sentences
Summary
Following KP-10 overexpression in KYSE150 EC cells, we observed inhibited cell growth, promoted apoptosis, decreased cell migration, reduced cancer stem cell properties, and suppressed EMT.
In this study, Kisspeptin-10 was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking Kisspeptin-10.
Report a problemFND-4019261202
03LabNot a test of Kisspeptin-10 aloneIn vitro (cells)Efficacy outcome
In KYSE150 esophageal cancer cells, KP-10 overexpression promoted apoptosis.
In plain wordsIn esophageal cancer cells in the lab, raising KP-10 production increased cell death.
Peptide
Kisspeptin-10
Outcome
IncreaseApoptosis after KP-10 overexpression
Study
n: not reported in source
KYSE150 esophageal cancer cells
Outcome group
Tumor growth · Cancer
Source sentences
Summary
Following KP-10 overexpression in KYSE150 EC cells, we observed inhibited cell growth, promoted apoptosis, decreased cell migration, reduced cancer stem cell properties, and suppressed EMT.
In this study, Kisspeptin-10 was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking Kisspeptin-10.
Report a problemFND-4019261203
04LabNot a test of Kisspeptin-10 aloneIn vitro (cells)Efficacy outcome
In KYSE150 esophageal cancer cells, KP-10 overexpression decreased cell migration.
In plain wordsIn esophageal cancer cells in the lab, raising KP-10 production reduced cell movement.
Peptide
Kisspeptin-10
Outcome
DecreaseCell migration after KP-10 overexpression
Study
n: not reported in source
KYSE150 esophageal cancer cells
Outcome group
Tumor growth · Cancer
Source sentences
Summary
Following KP-10 overexpression in KYSE150 EC cells, we observed inhibited cell growth, promoted apoptosis, decreased cell migration, reduced cancer stem cell properties, and suppressed EMT.
In this study, Kisspeptin-10 was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking Kisspeptin-10.
Report a problemFND-4019261204
05LabNot a test of Kisspeptin-10 aloneIn vitro (cells)Efficacy outcome
In KYSE150 esophageal cancer cells, KP-10 overexpression reduced cancer stem cell properties.
In plain wordsIn esophageal cancer cells in the lab, raising KP-10 production reduced stem-cell-like traits.
Peptide
Kisspeptin-10
Outcome
DecreaseCancer stem cell properties after KP-10 overexpression
Study
n: not reported in source
KYSE150 esophageal cancer cells
Outcome group
Tumor growth · Cancer
Source sentences
Summary
Following KP-10 overexpression in KYSE150 EC cells, we observed inhibited cell growth, promoted apoptosis, decreased cell migration, reduced cancer stem cell properties, and suppressed EMT.
In this study, Kisspeptin-10 was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking Kisspeptin-10.
Report a problemFND-4019261205
06LabNot a test of Kisspeptin-10 aloneIn vitro (cells)Mechanism
In KYSE150 esophageal cancer cells, KP-10 overexpression suppressed epithelial-mesenchymal transition.
In plain wordsIn esophageal cancer cells in the lab, raising KP-10 production reduced a change linked to cancer spread.
Peptide
Kisspeptin-10
Outcome
DecreaseEpithelial-mesenchymal transition after KP-10 overexpression
Study
n: not reported in source
KYSE150 esophageal cancer cells
Outcome group
Tumor growth · Cancer
Source sentences
Summary
Following KP-10 overexpression in KYSE150 EC cells, we observed inhibited cell growth, promoted apoptosis, decreased cell migration, reduced cancer stem cell properties, and suppressed EMT.
In this study, Kisspeptin-10 was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking Kisspeptin-10.
Report a problemFND-4019261206
07LabNot a test of Kisspeptin-10 aloneIn vitro (cells)Mechanism
In KYSE150 esophageal cancer cells, KP-10 overexpression inhibited the Wnt/β-catenin pathway, and SIX1 overexpression reversed this effect.
In plain wordsIn esophageal cancer cells in the lab, raising KP-10 production switched off the Wnt/β-catenin pathway, and SIX1 reversed this.
Peptide
Kisspeptin-10
Outcome
DecreaseWnt/β-catenin signaling after KP-10 overexpression
Study
n: not reported in source
KYSE150 esophageal cancer cells
Outcome group
Receptor activity and mechanism · Cancer
Source sentences
Summary
Furthermore, KP-10 overexpression inhibited the Wnt/β-catenin signaling pathway, an effect that was reversed by SIX1 overexpression, suggesting that KP-10's impact on this pathway is mediated through SIX1.
In this study, Kisspeptin-10 was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking Kisspeptin-10.
Report a problemFND-4019261207

AI wrote and checked these results. AI can make mistakes, so check important results against the source.

Version history

PepBank keeps every version of the data on this study. Status changes from Retraction Watch, Europe PMC and Crossref are listed with their source.

Version 2Current
10 Oct 2026, 09:43 UTC
Study results updated
Version 1
9 Oct 2026, 03:04 UTC
First added · source update from Europe PMC

Subjects

Terms as the source lists them.

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