ROS homeostasis and metabolism are critical for cancer progression, as tumor cells maintain high levels of reactive oxygen species (ROS) through genetic and metabolic alterations. These ROS levels, while harmful to normal cells, promote tumor growth by causing DNA damage, genomic instability, and reprogramming of cancer cell metabolism. Tumor cells have developed efficient mechanisms to detoxify ROS, relying on antioxidant systems like NADPH and GSH. This review highlights the role of mitochondria in regulating redox homeostasis and metabolism in cancer cells, and explores therapeutic strategies targeting metabolic pathways to disrupt redox balance and enhance cancer cell death. Tumor cells exhibit altered redox balance, with increased ROS levels and enhanced antioxidant capacity. This pro-oxidant shift can promote tumor growth by inducing DNA damage and activating inflammatory responses, which stabilize hypoxia-inducible factor-1 and reprogram metabolism. Cancer cells are vulnerable to oxidative stress, and therapies that increase ROS levels above the toxicity threshold can selectively kill cancer cells while sparing normal cells. Strategies to manipulate redox signaling, such as using metabolic inhibitors or pro-oxidizing agents, may enhance the effectiveness of conventional therapies like chemotherapy and radiotherapy. Metabolic pathways in cancer cells, including glycolysis, fatty acid oxidation, the pentose phosphate pathway, glutaminolysis, and one-carbon metabolism, are closely linked to redox homeostasis. These pathways generate reducing equivalents like NADPH and GSH, which are essential for maintaining redox balance and preventing oxidative damage. Targeting these pathways, particularly those involved in NADPH and GSH production, may offer new therapeutic approaches to disrupt cancer cell survival and promote cell death. Mitochondria play a central role in redox homeostasis and metabolism in cancer cells. They generate ROS through the mitochondrial electron transport chain and are involved in the production of NADPH and GSH. Targeting mitochondrial function, such as with compounds that inhibit the mitochondrial electron transport chain, may be a promising strategy for cancer therapy. Additionally, drugs like metformin and phenformin, which target mitochondrial bioenergetics, show potential in reducing tumor growth and enhancing the effectiveness of other therapies. The review emphasizes the importance of understanding the complex interplay between redox homeostasis and metabolism in cancer cells. By manipulating these pathways, it may be possible to develop more effective therapies that target cancer cells specifically while minimizing harm to normal cells. Future research should focus on identifying novel therapeutic strategies that exploit the unique metabolic and redox characteristics of cancer cells.ROS homeostasis and metabolism are critical for cancer progression, as tumor cells maintain high levels of reactive oxygen species (ROS) through genetic and metabolic alterations. These ROS levels, while harmful to normal cells, promote tumor growth by causing DNA damage, genomic instability, and reprogramming of cancer cell metabolism. Tumor cells have developed efficient mechanisms to detoxify ROS, relying on antioxidant systems like NADPH and GSH. This review highlights the role of mitochondria in regulating redox homeostasis and metabolism in cancer cells, and explores therapeutic strategies targeting metabolic pathways to disrupt redox balance and enhance cancer cell death. Tumor cells exhibit altered redox balance, with increased ROS levels and enhanced antioxidant capacity. This pro-oxidant shift can promote tumor growth by inducing DNA damage and activating inflammatory responses, which stabilize hypoxia-inducible factor-1 and reprogram metabolism. Cancer cells are vulnerable to oxidative stress, and therapies that increase ROS levels above the toxicity threshold can selectively kill cancer cells while sparing normal cells. Strategies to manipulate redox signaling, such as using metabolic inhibitors or pro-oxidizing agents, may enhance the effectiveness of conventional therapies like chemotherapy and radiotherapy. Metabolic pathways in cancer cells, including glycolysis, fatty acid oxidation, the pentose phosphate pathway, glutaminolysis, and one-carbon metabolism, are closely linked to redox homeostasis. These pathways generate reducing equivalents like NADPH and GSH, which are essential for maintaining redox balance and preventing oxidative damage. Targeting these pathways, particularly those involved in NADPH and GSH production, may offer new therapeutic approaches to disrupt cancer cell survival and promote cell death. Mitochondria play a central role in redox homeostasis and metabolism in cancer cells. They generate ROS through the mitochondrial electron transport chain and are involved in the production of NADPH and GSH. Targeting mitochondrial function, such as with compounds that inhibit the mitochondrial electron transport chain, may be a promising strategy for cancer therapy. Additionally, drugs like metformin and phenformin, which target mitochondrial bioenergetics, show potential in reducing tumor growth and enhancing the effectiveness of other therapies. The review emphasizes the importance of understanding the complex interplay between redox homeostasis and metabolism in cancer cells. By manipulating these pathways, it may be possible to develop more effective therapies that target cancer cells specifically while minimizing harm to normal cells. Future research should focus on identifying novel therapeutic strategies that exploit the unique metabolic and redox characteristics of cancer cells.