Reactive oxygen species (ROS) are highly reactive molecules with unpaired electrons, playing a critical role in cancer development and progression. While cancer cells produce high levels of ROS, they also express antioxidant proteins to maintain a balance, as excessive ROS can promote tumor growth. ROS are generated in various cellular compartments, including mitochondria, peroxisomes, and through signaling pathways involving growth factors and oncogenes. Mitochondria produce ROS as a byproduct of oxidative phosphorylation, while peroxisomes generate ROS via xanthine oxidase. ROS can also be produced by immune cells during inflammation, contributing to tumor cell apoptosis. Cancer cells detoxify ROS through non-enzymatic molecules and antioxidant enzymes such as superoxide dismutases (SODs), catalase, peroxiredoxins, and the glutathione system. These enzymes help maintain intracellular ROS levels, which are essential for cell survival and proliferation. However, excessive ROS can lead to oxidative stress, DNA damage, and apoptosis. ROS regulate key signaling pathways in cancer, including the MAPK/Erk, PI3K/Akt, and IKK/NF-κB pathways, which are involved in cell growth, survival, and metastasis. ROS also influence cell motility, angiogenesis, and the maintenance of cancer stem cells. ROS can promote tumor progression by enhancing cell proliferation, survival, and metastasis, while also contributing to genomic instability and DNA damage. However, therapeutic strategies targeting ROS can be beneficial by modulating ROS levels to induce apoptosis or prevent tumor development. Antioxidants and compounds that increase ROS levels are being explored as potential cancer therapies. Additionally, ROS play a role in angiogenesis, which is crucial for tumor growth and metastasis. Understanding the complex roles of ROS in cancer is essential for developing effective therapeutic approaches.Reactive oxygen species (ROS) are highly reactive molecules with unpaired electrons, playing a critical role in cancer development and progression. While cancer cells produce high levels of ROS, they also express antioxidant proteins to maintain a balance, as excessive ROS can promote tumor growth. ROS are generated in various cellular compartments, including mitochondria, peroxisomes, and through signaling pathways involving growth factors and oncogenes. Mitochondria produce ROS as a byproduct of oxidative phosphorylation, while peroxisomes generate ROS via xanthine oxidase. ROS can also be produced by immune cells during inflammation, contributing to tumor cell apoptosis. Cancer cells detoxify ROS through non-enzymatic molecules and antioxidant enzymes such as superoxide dismutases (SODs), catalase, peroxiredoxins, and the glutathione system. These enzymes help maintain intracellular ROS levels, which are essential for cell survival and proliferation. However, excessive ROS can lead to oxidative stress, DNA damage, and apoptosis. ROS regulate key signaling pathways in cancer, including the MAPK/Erk, PI3K/Akt, and IKK/NF-κB pathways, which are involved in cell growth, survival, and metastasis. ROS also influence cell motility, angiogenesis, and the maintenance of cancer stem cells. ROS can promote tumor progression by enhancing cell proliferation, survival, and metastasis, while also contributing to genomic instability and DNA damage. However, therapeutic strategies targeting ROS can be beneficial by modulating ROS levels to induce apoptosis or prevent tumor development. Antioxidants and compounds that increase ROS levels are being explored as potential cancer therapies. Additionally, ROS play a role in angiogenesis, which is crucial for tumor growth and metastasis. Understanding the complex roles of ROS in cancer is essential for developing effective therapeutic approaches.