Аңдатпа
Resistance to cancer therapy remains a major limitation in oncology, often leading to disease progression despite an initial response to treatment. One of the key factors underlying this phenomenon is the ability of cancer cells to adapt to oxidative stress. Many anticancer therapies rely on the generation of reactive oxygen species (ROS) to induce cell death, yet tumor cells can counteract this effect by strengthening their antioxidant capacity and adjusting redox-related pathways. This review focuses on how redox homeostasis is altered in cancer and how these changes support survival under therapeutic pressure. It discusses the role of major antioxidant systems, including glutathione and thioredoxin, as well as transcriptional regulators such as NRF2, HIF-1α, and NF-κB. In addition, it highlights how ROS influence key processes in tumor progression, including proliferation, apoptosis evasion, angiogenesis, and metastasis. Therapeutic approaches aimed at disrupting redox balance are also discussed, including strategies that either increase ROS levels or interfere with antioxidant systems and endoplasmic reticulum enzymes such as ERO1α and protein disulfide isomerase. While these approaches have shown encouraging results in experimental settings, their translation into clinical use is still constrained by issues related to selectivity and the emergence of resistance. Combining redox-targeting agents with standard treatments may offer a more practical way to enhance their effectiveness and improve patient outcomes.