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Updated: Jan 29, 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

71.0K

Adverse Outcome Pathway 298: Increase in Reactive Oxygen Species Leading to Human Treatment-Resistant Gastric Cancer

Shihori Tanabe1, Sabina Quader2, Ryuichi Ono3

  • 1Division of Risk Assessment, Center for Biological Safety and Research, National Institute of Health Sciences, 3-25-26, Tonomachi, Kawasaki-ku, Kawasaki 210-9501, Japan.

Cancers
|January 28, 2026
PubMed

Insights

Increased reactive oxygen species (ROS) drive treatment resistance in human gastric cancer by activating Wnt/beta-catenin signaling and epithelial-mesenchymal transition (EMT). This pathway highlights a key mechanism for gastric cancer therapy resistance.

Area of Science:

  • Oncology
  • Molecular Biology
  • Toxicology

Background:

  • Gastric cancer exhibits resistance to treatments.
  • Adverse Outcome Pathway (AOP) 298 links increased reactive oxygen species (ROS) to treatment-resistant gastric cancer.
  • ROS plays multifaceted roles in cancer, including progression and apoptosis induction.

Purpose of the Study:

  • To elucidate the role of sustained chronic ROS levels in inducing therapy resistance in human gastric cancer.
  • To detail the sequence of events in AOP 298, from ROS increase to treatment resistance.

Main Methods:

  • The study outlines Adverse Outcome Pathway (AOP) 298, detailing key events and relationships.
  • Focuses on the molecular initiating event (MIE) of increased ROS and subsequent key events (KEs).
  • Examines the pathway involving porcupine-induced Wnt secretion, beta-catenin activation, and epithelial-mesenchymal transition (EMT).

Main Results:

  • AOP 298 describes a causal chain: increased ROS → Wnt signaling activation → beta-catenin activation → EMT → treatment-resistant gastric cancer.
  • Sustained chronic ROS levels are identified as a driver of therapy resistance in gastric cancer.
  • EMT, mediated by Wnt/beta-catenin signaling, confers cancer stem cell-like characteristics.

Conclusions:

  • The Wnt/beta-catenin signaling pathway and subsequent EMT are critical mediators of ROS-induced gastric cancer treatment resistance.
  • Understanding AOP 298 provides insights into mechanisms of therapeutic failure in gastric cancer.
  • Targeting ROS or downstream pathways like Wnt/beta-catenin/EMT may offer strategies to overcome treatment resistance.
Keywords:
Wnt signalingadverse outcome pathway (AOP)epithelial–mesenchymal transition (EMT)gastric cancerreactive oxygen species (ROS)

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