Mitochondria play a critical role in cancer therapy due to their involvement in ATP production, biosynthesis, and signaling. Historically, mitochondria were thought to be irrelevant to cancer cell metabolism, but recent studies show that mitochondrial metabolism is essential for tumorigenesis. Cancer cells use both glycolysis and mitochondrial metabolism to generate energy and biosynthetic intermediates. Mitochondria also produce reactive oxygen species (ROS), which can promote genetic instability and tumorigenesis. However, cancer cells have mechanisms to manage ROS levels and prevent cell death. Mitochondrial metabolism is crucial for tumor growth, as it provides energy and biosynthetic precursors. Tumor cells often rely on glucose and glutamine for energy and macromolecule synthesis. Mitochondrial dysfunction can lead to increased ROS production, which activates signaling pathways that promote cancer cell proliferation. However, cancer cells also have ways to manage ROS levels through NADPH production and antioxidant systems. Targeting mitochondrial metabolism for cancer therapy is a promising approach. Metformin, an antidiabetic drug, has shown potential as an anticancer agent by inhibiting mitochondrial complex I, reducing ATP production, and inducing cell death. Other drugs, such as phenformin, also inhibit mitochondrial complex I and have shown antitumor effects. Additionally, targeting mitochondrial biosynthetic functions, such as glutamine metabolism, and mitochondrial redox capacity can be effective strategies. Mitochondrial dysfunction is a key factor in cancer, and targeting mitochondrial metabolism offers a new avenue for cancer treatment. However, challenges remain in translating these findings into clinical applications, including ensuring the safety of mitochondrial-targeted therapies and understanding the basic biology of mitochondrial metabolism in tumorigenesis. Overall, mitochondrial metabolism is a promising target for cancer therapy, with ongoing research exploring its potential as a therapeutic strategy.Mitochondria play a critical role in cancer therapy due to their involvement in ATP production, biosynthesis, and signaling. Historically, mitochondria were thought to be irrelevant to cancer cell metabolism, but recent studies show that mitochondrial metabolism is essential for tumorigenesis. Cancer cells use both glycolysis and mitochondrial metabolism to generate energy and biosynthetic intermediates. Mitochondria also produce reactive oxygen species (ROS), which can promote genetic instability and tumorigenesis. However, cancer cells have mechanisms to manage ROS levels and prevent cell death. Mitochondrial metabolism is crucial for tumor growth, as it provides energy and biosynthetic precursors. Tumor cells often rely on glucose and glutamine for energy and macromolecule synthesis. Mitochondrial dysfunction can lead to increased ROS production, which activates signaling pathways that promote cancer cell proliferation. However, cancer cells also have ways to manage ROS levels through NADPH production and antioxidant systems. Targeting mitochondrial metabolism for cancer therapy is a promising approach. Metformin, an antidiabetic drug, has shown potential as an anticancer agent by inhibiting mitochondrial complex I, reducing ATP production, and inducing cell death. Other drugs, such as phenformin, also inhibit mitochondrial complex I and have shown antitumor effects. Additionally, targeting mitochondrial biosynthetic functions, such as glutamine metabolism, and mitochondrial redox capacity can be effective strategies. Mitochondrial dysfunction is a key factor in cancer, and targeting mitochondrial metabolism offers a new avenue for cancer treatment. However, challenges remain in translating these findings into clinical applications, including ensuring the safety of mitochondrial-targeted therapies and understanding the basic biology of mitochondrial metabolism in tumorigenesis. Overall, mitochondrial metabolism is a promising target for cancer therapy, with ongoing research exploring its potential as a therapeutic strategy.