The study investigates the role of lactate in tumor metabolism and its potential as a therapeutic target. Lactate, produced by glycolysis in hypoxic tumor cells, is taken up by oxidative tumor cells via monocarboxylate transporter 1 (MCT1) and used for oxidative metabolism. This symbiotic relationship allows hypoxic cells to survive while sparing glucose for oxidative cells. The researchers found that inhibiting MCT1 with α-cyano-4-hydroxycinnamate (CHC) or siRNA in oxidative tumor cells switched their metabolism from lactate to glucose, leading to cell death due to glucose starvation. This switch also increased tumor oxygenation, making the remaining cells more sensitive to radiation. In vivo experiments in mouse models of lung and liver cancer showed that MCT1 inhibition delayed tumor growth and induced necrosis. MCT1 is expressed in various human tumors, suggesting that MCT1 inhibition has clinical potential as an anticancer treatment alone or in combination with radiotherapy.The study investigates the role of lactate in tumor metabolism and its potential as a therapeutic target. Lactate, produced by glycolysis in hypoxic tumor cells, is taken up by oxidative tumor cells via monocarboxylate transporter 1 (MCT1) and used for oxidative metabolism. This symbiotic relationship allows hypoxic cells to survive while sparing glucose for oxidative cells. The researchers found that inhibiting MCT1 with α-cyano-4-hydroxycinnamate (CHC) or siRNA in oxidative tumor cells switched their metabolism from lactate to glucose, leading to cell death due to glucose starvation. This switch also increased tumor oxygenation, making the remaining cells more sensitive to radiation. In vivo experiments in mouse models of lung and liver cancer showed that MCT1 inhibition delayed tumor growth and induced necrosis. MCT1 is expressed in various human tumors, suggesting that MCT1 inhibition has clinical potential as an anticancer treatment alone or in combination with radiotherapy.