Reactive oxygen species (ROS) are highly reactive molecules involved in cellular signaling and regulation. While moderate levels of ROS are essential for normal cellular functions, excessive ROS can cause oxidative stress, leading to DNA damage, mutations, and cancer progression. However, ROS also play a critical role in inducing programmed cell death (PCD), including apoptosis, autophagy, and necroptosis, which can be harnessed for cancer therapy. The review highlights the dual role of ROS in cancer, emphasizing their potential as therapeutic targets. ROS are generated through various metabolic pathways, including mitochondrial respiration, peroxisomal β-oxidation, and endoplasmic reticulum protein oxidation. They are also produced by enzymatic reactions such as those involving NADPH oxidases, xanthine oxidases, and lipoxygenases. ROS can influence cellular signaling by modifying proteins, altering transcription factors, and affecting gene expression. Key transcription factors like Nrf2, FOXO, and p53 regulate antioxidant responses and cell survival, while ROS can also promote cancer progression by enhancing angiogenesis, epithelial-mesenchymal transition, and metastasis. ROS-induced DNA damage, such as 8-oxo-G, can lead to mutations and chromosomal abnormalities, contributing to cancer development. ROS also influence epigenetic modifications, including DNA methylation and histone acetylation, which can alter gene expression patterns. Additionally, ROS can induce mitochondrial dysfunction, leading to cell death through mechanisms such as ferroptosis, which is dependent on intracellular iron and ROS levels. Cancer cells often develop increased antioxidant systems to manage ROS levels, making them more susceptible to further ROS induction. Therapeutic strategies targeting ROS include drugs that increase ROS production, such as those that inhibit antioxidant enzymes or disrupt mitochondrial function. These approaches aim to induce oxidative stress and cell death in cancer cells while minimizing damage to normal cells. Photodynamic therapy, which uses light-activated photosensitizers to generate ROS, is another promising approach. The review underscores the importance of understanding the complex interplay between ROS and cancer, highlighting the potential of ROS-based therapies in cancer treatment. While antioxidant therapies have shown mixed results, recent studies suggest that targeting ROS production may be more effective in cancer therapy. The dual role of ROS as both a harmful and beneficial factor in cancer highlights the need for careful modulation of ROS levels to achieve therapeutic success.Reactive oxygen species (ROS) are highly reactive molecules involved in cellular signaling and regulation. While moderate levels of ROS are essential for normal cellular functions, excessive ROS can cause oxidative stress, leading to DNA damage, mutations, and cancer progression. However, ROS also play a critical role in inducing programmed cell death (PCD), including apoptosis, autophagy, and necroptosis, which can be harnessed for cancer therapy. The review highlights the dual role of ROS in cancer, emphasizing their potential as therapeutic targets. ROS are generated through various metabolic pathways, including mitochondrial respiration, peroxisomal β-oxidation, and endoplasmic reticulum protein oxidation. They are also produced by enzymatic reactions such as those involving NADPH oxidases, xanthine oxidases, and lipoxygenases. ROS can influence cellular signaling by modifying proteins, altering transcription factors, and affecting gene expression. Key transcription factors like Nrf2, FOXO, and p53 regulate antioxidant responses and cell survival, while ROS can also promote cancer progression by enhancing angiogenesis, epithelial-mesenchymal transition, and metastasis. ROS-induced DNA damage, such as 8-oxo-G, can lead to mutations and chromosomal abnormalities, contributing to cancer development. ROS also influence epigenetic modifications, including DNA methylation and histone acetylation, which can alter gene expression patterns. Additionally, ROS can induce mitochondrial dysfunction, leading to cell death through mechanisms such as ferroptosis, which is dependent on intracellular iron and ROS levels. Cancer cells often develop increased antioxidant systems to manage ROS levels, making them more susceptible to further ROS induction. Therapeutic strategies targeting ROS include drugs that increase ROS production, such as those that inhibit antioxidant enzymes or disrupt mitochondrial function. These approaches aim to induce oxidative stress and cell death in cancer cells while minimizing damage to normal cells. Photodynamic therapy, which uses light-activated photosensitizers to generate ROS, is another promising approach. The review underscores the importance of understanding the complex interplay between ROS and cancer, highlighting the potential of ROS-based therapies in cancer treatment. While antioxidant therapies have shown mixed results, recent studies suggest that targeting ROS production may be more effective in cancer therapy. The dual role of ROS as both a harmful and beneficial factor in cancer highlights the need for careful modulation of ROS levels to achieve therapeutic success.