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Updated: Feb 11, 2026

Production and Detection of Reactive Oxygen Species ROS in Cancers
07:17

Production and Detection of Reactive Oxygen Species ROS in Cancers

Published on: November 21, 2011

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Melatonin Inhibits Reactive Oxygen Species-Driven Proliferation, Epithelial-Mesenchymal Transition, and Vasculogenic

Rui Liu1,2,3, Hui-Li Wang4, Man-Jing Deng1

  • 1Department of Stomatology, Daping Hospital and Research Institute of Surgery, Third Military Medical University, Chongqing 400042, China.

Oxidative Medicine and Cellular Longevity
|May 5, 2018
PubMed

Insights

Melatonin inhibits oral cancer growth by reducing cell survival, migration, and blood vessel formation. These effects are mediated by blocking reactive oxygen species (ROS)-dependent Akt and ERK signaling pathways.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Oral cancer is a prevalent head and neck malignancy.
  • Melatonin shows potential in inhibiting oral cancer, but its mechanisms are unclear.

Purpose of the Study:

  • To investigate the biological functions and mechanisms of melatonin in oral cancer.
  • To elucidate how melatonin affects oral cancer cell proliferation, apoptosis, migration, invasion, and vasculogenic mimicry.

Main Methods:

  • In vitro studies on oral cancer cells to assess proliferation, apoptosis, migration, and invasion.
  • Analysis of signaling pathways including ROS-dependent Akt and ERK.
  • In vivo studies to evaluate melatonin's effect on tumor growth.

Main Results:

  • Melatonin impaired oral cancer cell proliferation and apoptosis resistance via ROS-dependent Akt inactivation.
  • Melatonin inhibited oral cancer cell migration and invasion by repressing ROS-activated Akt signaling.
  • Melatonin hampered vasculogenic mimicry by blocking ROS-activated ERK and Akt pathways.
  • Melatonin retarded oral cancer tumorigenesis in vivo.

Conclusions:

  • Melatonin exhibits antisurvival, antimotility, and antiangiogenesis effects on oral cancer.
  • These effects are partly mediated by suppressing ROS-reliant Akt or ERK signaling pathways.

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