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Updated: Jun 29, 2026
Production and Detection of Reactive Oxygen Species (ROS) in Cancers
Published on: November 21, 2011
Regulation of autophagy by reactive oxygen species (ROS): implications for cancer progression and treatment
Meghan B Azad1, Yongqiang Chen, Spencer B Gibson
1Manitoba Institute of Cell Biology, Faculty of Medicine, University of Manitoba, Winnipeg, Manitoba, Canada.
Abstract:
Reactive oxygen species (ROS) have been identified as signaling molecules in various pathways regulating both cell survival and cell death. Autophagy, a self-digestion process that degrades intracellular structures in response to stress, such as nutrient starvation, is also involved in both cell survival and cell death. Alterations in both ROS and autophagy regulation contribute to cancer initiation and progression, and both are targets for developing therapies to induce cell death selectively in cancer cells. Many stimuli that induce ROS generation also induce autophagy, including nutrient starvation, mitochondrial toxins, hypoxia, and oxidative stress. Some of these stimuli are under clinical investigation as cancer treatments, such as 2-methoxyestrodial and arsenic trioxide. Recently, it was demonstrated that ROS can induce autophagy through several distinct mechanisms involving Atg4, catalase, and the mitochondrial electron transport chain (mETC). This leads to both cell-survival and cell-death responses and could be selective toward cancer cells. In this review, we give an overview of the roles ROS and autophagy play in cell survival and cell death, and their importance to cancer. Furthermore, we describe how autophagy is mediated by ROS and the implications of this regulation to cancer treatments.
Insights
Reactive oxygen species (ROS) and autophagy are key regulators of cell death and survival. Their interplay offers a promising strategy for developing targeted cancer therapies by selectively inducing cancer cell death.
Area of Science:
- Cell Biology
- Biochemistry
- Oncology
Background:
- Reactive oxygen species (ROS) act as signaling molecules influencing cell survival and death pathways.
- Autophagy, a cellular self-digestion process, also plays a dual role in cell fate.
- Dysregulation of ROS and autophagy is implicated in cancer development and progression.
Purpose of the Study:
- To review the roles of ROS and autophagy in cell survival and death.
- To explore the significance of ROS and autophagy in cancer.
- To describe ROS-mediated autophagy mechanisms and their therapeutic implications for cancer.
Main Methods:
- Literature review of studies on ROS, autophagy, and cancer.
- Analysis of signaling pathways linking ROS generation and autophagy induction.
- Examination of stimuli that trigger both ROS and autophagy.
Main Results:
- ROS and autophagy are involved in both pro-survival and pro-death cellular responses.
- Numerous stimuli, including nutrient starvation and hypoxia, induce both ROS and autophagy.
- ROS can initiate autophagy via mechanisms involving Atg4, catalase, and the mitochondrial electron transport chain (mETC).
Conclusions:
- The intricate relationship between ROS and autophagy presents potential for selective cancer cell death induction.
- Understanding ROS-mediated autophagy is crucial for developing novel cancer therapeutics.
- Targeting the ROS-autophagy axis may offer selective therapeutic strategies against cancer.
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