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REVIEW

The Role of Mitochondrial ROS in Neoplastic Transformations, Progression and Therapeutic Targeting

Bharath Kumar Velmurugan1, Shu Hui Lin2,3,4, Chih-Yang Huang5,6,7,8,9,10, Ming-Ju Hsieh9,11,12,*, Rathinasamy Baskaran10,*
1 Maitocon Laboratory, Tirupur, Tamil Nadu, India
2 Department of Surgical Pathology, Changhua Christian Hospital, Changhua, Taiwan
3 Department of Medical Laboratory Science and Biotechnology, Central Taiwan University of Science and Technology, Taichung, Taiwan
4 Department of Post-Baccalaureate Medicine, College of Medicine, National Chung Hsing University, Taichung, Taiwan
5 Department of Precision Chinese Herbal Medicine and Molecular Medicine Research, E-Da Cancer Hospital, E-Da Healthcare Group, Kaohsiung, Taiwan
6 School of Chinese Medicine for Post Baccalaureate, I-Shou University, Kaohsiung, Taiwan
7 Department of Medical Research, China Medical University Hospital, China Medical University, Taichung, Taiwan
8 Department of Medical Laboratory Science and Biotechnology, Asia University, Taichung, Taiwan
9 Graduate Institute of Biomedical Sciences, China Medical University, Taichung, Taiwan
10 Cardiovascular and Mitochondrial Related Disease Research Center, Hualien Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, Hualien, Taiwan
11 Oral Cancer Research Center, Changhua Christian Hospital, Changhua, Taiwan
12 Graduate Institute of Clinical Medicine, College of Medicine, National Chung Hsing University, Taichung, Taiwan
* Corresponding Author: Ming-Ju Hsieh. Email: email; Rathinasamy Baskaran. Email: email

Oncology Research https://doi.org/10.32604/or.2026.083159

Received 30 March 2026; Accepted 10 June 2026; Published online 08 July 2026

Abstract

Mitochondria are central regulators of cellular metabolism and survival and play a pivotal role in cancer development and progression through the production of reactive oxygen species (ROS), control of calcium homeostasis, regulation of autophagy, and modulation of cell death pathways. Mitochondria-derived ROS (mtROS) act as signaling mediators that influence tumor initiation, proliferation, metabolic reprogramming, metastasis, and therapeutic resistance by altering redox homeostasis, damaging mitochondrial DNA, and reshaping the tumor microenvironment. In addition to meeting the bioenergetic and biosynthetic requirements of rapidly proliferating cancer cells, mitochondrial metabolism modulates immune responses and supports cancer cell adaptation to hypoxia and nutrient deprivation. Accumulating evidence also highlights the dual role of mtROS, which can promote tumor progression at moderate levels yet trigger oxidative stress-induced cell death when excessively increased, making mitochondrial redox signaling an attractive therapeutic target. This review summarizes the major sources and regulation of mtROS, their involvement in cancer-associated signaling pathways, mitochondrial calcium dynamics, metabolic adaptations, and resistance to anticancer therapies, and discusses current and emerging mitochondrial-targeted strategies aimed at exploiting mtROS signaling to improve cancer treatment outcomes.

Keywords

Cancer; reactive oxygen species; mitochondria; oncometabolites; electron transport chain

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