Reactive oxygen species in cancer: Mechanistic insights and therapeutic innovations.

Reactive oxygen species (ROS), once considered mere metabolic byproducts, are now recognized as crucial elements in the complex behavior of cancer, influencing both its progression and vulnerabilities. In healthy cells, ROS maintains a delicate balance: while small amounts are essential for signaling, excessive quantities can cause damage. Cancer disrupts this equilibrium, leveraging ROS to promote proliferation, metastasis, and survival, while employing antioxidant defenses to prevent self-destruction. It is the balance of ROS that is key to cancer growth: as they initiate cancer-related processes such as Mitogen-Activated Protein Kinase (MAPK), PI3K/Akt, and c-Jun N-terminal Kinase (JNK) pathways, and induce inflammation through NF-κB. Additionally, matrix metalloproteinases (MMPs) and vascular endothelial growth factor (VEGF) break down tissue barriers, fostering a tumor microenvironment (TME) conducive to cancer spread. However, this dependence on ROS presents a dual challenge. The timing, location, and quantity of radical formation, along with the surrounding cellular environment, determine whether ROS facilitate cancer progression or lead to cancer cell death. Disrupting this delicate balance of ROS may reveal new treatment methods, transforming cancer's survival mechanisms into significant weaknesses. This study explores the dual roles of ROS in cancer, examining how their contrasting effects impact tumor growth and revealing unexpected opportunities to shift the balance from growth to vulnerability.