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Updated: Oct 7, 2025

Mutagenesis and Analysis of Genetic Mutations in the GC-rich KISS1 Receptor Sequence Identified in Humans with Reproductive Disorders
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Mutagenesis and Analysis of Genetic Mutations in the GC-rich KISS1 Receptor Sequence Identified in Humans with Reproductive Disorders

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KISS-1, Mediated by Promoter Methylation, Suppresses Esophageal Squamous Cell Carcinoma Metastasis via MMP2/9/MAPK

Houyu Duan1, Xiang Ding1, Hesheng Luo2

  • 1Department of Gastroenterology, Renmin Hospital of Wuhan University, Wuhan, 430060, Hubei, People's Republic of China.

Digestive Diseases and Sciences
|January 7, 2022
PubMed
Abstract

Insights

KISS-1, a tumor suppressor, is downregulated in esophageal squamous cell carcinoma (ESCC) due to promoter hypermethylation. Restoring KISS-1 inhibits ESCC metastasis by targeting MMP2/9/ERK/p38 MAPK signaling.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Metastasis Research

Background:

  • KISS-1 is a known tumor suppressor with anti-metastatic properties.
  • Its specific role and mechanisms in esophageal squamous cell carcinoma (ESCC) remain largely unexplored.

Purpose of the Study:

  • To investigate the role of KISS-1 in ESCC metastasis.
  • To elucidate the underlying molecular mechanisms by which KISS-1 influences ESCC progression.

Main Methods:

  • Analysis of KISS-1 mRNA and protein expression in ESCC tissues and cell lines using qRT-PCR, IHC, and Western blotting.
  • Assessment of KISS-1 promoter methylation patterns via BSP and MSP.
  • In vitro functional assays to evaluate the impact of KISS-1 on ESCC cell metastasis and epithelial-mesenchymal transition (EMT).

Main Results:

  • KISS-1 expression was significantly downregulated in ESCC tissues and cell lines.
  • Promoter hypermethylation correlated with reduced KISS-1 levels; demethylation suppressed tumor progression.
  • Overexpression of KISS-1 inhibited ESCC cell metastasis, downregulated matrix metalloproteinases (MMP2 and 9), and suppressed EMT.
  • KISS-1 reduced phosphorylated ERK1/2 and p38 MAPK, which was reversed by pathway agonists.

Conclusions:

  • Hypermethylation of the KISS-1 promoter is a contributing factor to its downregulation in ESCC.
  • KISS-1 suppresses ESCC cell metastasis through the MMP2/9/ERK/p38 MAPK signaling axis.
Keywords:
ESCCKISS-1MAPKMMPsMetastasisMethylation

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