Authors
Qing Tang, Lei Cui, Wei Du, Yuxia Ruan, Linhao Yang, Chunlin Fu, Jingqi Gui, Quentin Liu, Yibing Chen, Jianghua Qiao, Zhengzhi Zou
Published in
Journal of advanced research. Jul 05, 2026. Epub Jul 05, 2026.
Abstract
Reactive oxygen species (ROS) play a complex dual role in cancer biology. At physiological levels, ROS act as signaling molecules that drive tumorigenesis, metastasis, and therapy resistance by activating oncogenic pathways, such as NF-κB and PI3K/AKT, and fostering an immunosuppressive microenvironment. Conversely, excessive ROS accumulation overwhelms antioxidant defenses, triggering oxidative stress that can selectively eliminate tumor cells. Consequently, manipulating the delicate redox equilibrium has emerged as a pivotal strategy for cancer treatment.
This review systematically examines the multifaceted functions of ROS, bridging the gap between fundamental redox biology and clinical application within the Predictive, Preventive, and Personalized Medicine (3PM) framework. Beyond molecular mechanisms, we evaluated the rationale for utilizing mitochondrial redox signatures as intrinsic biological sensors to identify suboptimal health conditions (SHC) and prevent the health-to-disease transition.
We elucidate the regulatory networks governing ROS production and elimination, highlighting their dual function in promoting genomic instability versus inducing distinct cell death modalities, including apoptosis, autophagy, necroptosis, and ferroptosis. Special attention is given to ROS-mediated remodeling of the tumor microenvironment (TME), where oxidative stress facilitates immunosuppression. Importantly, we provide expert recommendations on integrating digital health monitoring and patient stratification into clinical oncology. By emphasizing mitochondrial rejuvenation and individualised protection, this review discusses how proactive interventions can restore homeostasis and improve long-term outcomes, offering a cost-effective alternative to reactive treatments.
PMID:
42402325
Bibliographic data and abstract were imported from PubMed on 06 Jul 2026.
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