Objective: One of the hallmarks of cancer is the aerobic glycolysis of glucose, the Warburg effect. For the same reason, solid tumors including the aggressive thyroid cancer develop resistance to cell death. We examined the possibility that targeting energy metabolism such as aerobic glycolysis is a potential strategy for anaplastic thyroid cancer treatment. Methods: We employed dichloroacetate (DCA), an inhibitor of pyruvate dehydrogenase kinase (PDK), to shift the glucose metabolism from aerobic glycolysis to normal glucose metabolism. We determined the cell viability and cell cycle by FACS analysis and also checked the expression levels of some genes involved in the glucose metabolism and cell cycle regulation. Results: DCA enhanced production of reactive oxygen species (ROS), ROS involvement was confirmed by ROS scavenger N-acetyl-Cysteine (NAC) pretreatment, which customarily inhibited the effect of DCA alone. Cell viability assay demonstrated that DCA had selective cytotoxicity against human ATC cell line. Flow cytometry and western blot analysis showed that the apoptosis was followed by cell cycle arrest in G1 phase. Conclusion: Taken together, DCA promotes induction of G1 cell cycle arrest and ROS production/intrinsic pathway of apoptosis in 8505-C. These results suggest that PDK is a good candidate to develop a therapeutic drug of anaplastic thyroid cancer.