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Kisspeptin Signaling Suppresses HRasG12V-induced Tumor Growth and Metastasis by Inhibiting SP1-dependent N-cadherin

Hyun-Ha Hwang1, Sung-Gook Cho2

  • 1Department of Science in Korean Medicine, Graduate School, College of Korean Medicine, Kyung Hee University, Seoul, Republic of Korea.

Anticancer Research
|July 29, 2026
PubMed
Abstract

Insights

Kisspeptin signaling suppresses HRAS-driven tumor growth and metastasis. This pathway inhibits N-cadherin transcription, a key factor in tumor progression.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Kisspeptin signaling is a known metastasis suppressor.
  • Its role in HRAS-driven cancers is not fully understood.
  • HRAS mutations drive tumor progression and metastasis.

Purpose of the Study:

  • Investigate kisspeptin's effect on HRASG12V-induced tumors.
  • Determine kisspeptin's impact on N-cadherin transcription.
  • Elucidate the role of SP1 in this pathway.

Main Methods:

  • NIH3T3 cells expressing HRASG12V, KISS1, and KISS1R were used.
  • Assays included proliferation, migration, invasion, and anchorage-independent growth.
  • N-cadherin expression and promoter activity were analyzed via RT-PCR, immunoblotting, luciferase reporters, and ChIP.

Main Results:

  • Kisspeptin signaling reduced proliferation, migration, and invasion.
  • Kisspeptin suppressed HRASG12V-induced N-cadherin expression and colony formation.
  • Kisspeptin inhibited SP1-dependent N-cadherin transcription, reducing tumor growth and metastasis.

Conclusions:

  • Kisspeptin signaling suppresses HRASG12V-induced tumor growth and metastasis.
  • This suppression occurs via inhibition of SP1-dependent N-cadherin transcription.
  • N-cadherin is a critical mediator in kisspeptin's anti-metastatic effects.
Keywords:
CancerRAScadherinkisspeptinmetastasis

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