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Updated: Feb 24, 2026
Production and Detection of Reactive Oxygen Species ROS in Cancers
Published on: November 21, 2011
Stressing the (Epi)Genome: Dealing with Reactive Oxygen Species in Cancer
Akshay V Bhat1, Shainan Hora2,3, Ananya Pal1
11 Department of Physiology, Yong Loo Lin School of Medicine, National University of Singapore , Singapore .
Significance:
Growing evidence indicates cross-talk between reactive oxygen species (ROS) and several key epigenetic processes such as DNA methylation, histone modifications, and miRNAs in normal physiology and human pathologies including cancer. This review focuses on how ROS-induced oxidative stress, metabolic intermediates, and epigenetic processes influence each other in various cancers. Recent Advances: ROS alter chromatin structure and metabolism that impact the epigenetic landscape in cancer cells. Several site-specific DNA methylation changes have been identified in different cancers and are discussed in the review. We also discuss the interplay of epigenetic enzymes and miRNAs in influencing malignant transformation in an ROS-dependent manner.
Critical Issues:
Loss of ROS-mediated signaling mostly by epigenetic regulation may promote tumorigenesis. In contrast, augmented oxidative stress because of high ROS levels may precipitate epigenetic alterations to effect various phases of carcinogenesis. We address both aspects in the review.
Future Directions:
Several drugs targeting ROS are under various stages of clinical development. Recent analysis of human cancers has revealed pervasive deregulation of the epigenetic machinery. Thus, a better understanding of the cross-talk between ROS and epigenetic alterations in cancer could lead to the identification of new drug targets and more effective treatment modalities.
Insights
Reactive oxygen species (ROS) and epigenetic changes interact in cancer. Understanding this cross-talk can reveal new drug targets for cancer treatment.
Area of Science:
- Oncology
- Epigenetics
- Oxidative Stress
Background:
- Reactive oxygen species (ROS) and epigenetic processes like DNA methylation, histone modifications, and microRNAs (miRNAs) are increasingly recognized for their interplay in normal physiology and cancer.
- This review explores the intricate relationship between ROS-induced oxidative stress, metabolic intermediates, and epigenetic modifications within various cancer types.
Purpose of the Study:
- To elucidate the mechanisms by which ROS and epigenetic alterations influence each other in cancer development and progression.
- To highlight the dual role of ROS in tumorigenesis, encompassing both loss of ROS-mediated signaling and augmented oxidative stress.
Main Methods:
- Review of current literature on the cross-talk between ROS and epigenetic mechanisms in cancer.
- Analysis of recent advances in understanding ROS-driven alterations in chromatin structure and cellular metabolism.
- Discussion of identified site-specific DNA methylation changes and the role of epigenetic enzymes and miRNAs in ROS-dependent malignant transformation.
Main Results:
- ROS significantly impact the epigenetic landscape of cancer cells by altering chromatin structure and metabolism.
- Specific DNA methylation changes are associated with various cancers, influenced by ROS levels.
- Epigenetic enzymes and miRNAs play a crucial role in malignant transformation in a ROS-dependent manner.
Conclusions:
- Both the loss and augmentation of ROS signaling, modulated by epigenetic regulation, can drive tumorigenesis.
- Understanding the complex interplay between ROS and epigenetic alterations is critical for identifying novel therapeutic targets.
- This knowledge may lead to the development of more effective cancer treatment strategies by targeting the ROS-epigenetic axis.
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