Rui V. Simoes1,
Ellen Ackestaff1, Inna Serganova2, Alexander A. Shestov3,
Natalia Kruchevsky1, George Sukenick4, Ronald G.
Blasberg2, 5, Jason A. Koutcher1, 6
1Medical
Physics, Memorial Sloan Kettering Cancer Center, New York, NY, United States;
2Neurology, Memorial Sloan Kettering Cancer Center, New York, NY,
United States; 3Division of Nutritional Sciences, Cornell
University, Ithaca, NY, United States; 4NMR Core Facility,
Memorial Sloan Kettering Cancer Center, New York, NY, United States; 5Radiology,
Memorial Sloan Kettering Cancer Center, New York, NY, United States; 6Weill
Cornell Medical College, Cornell University, New York, NY, United States
Recent work with two isogenic breast cancer cell lines, 4T1 (highly metastatic) and 67NR (non-metastatic), showed that 4T1 cells have higher glycolytic activity and oxygen consumption than 67NR, although revealing no significant differences in relative growth in response to glucose and/or glutamine deprivation. Here we investigated the mitochondrial metabolism of both cell lines, using 13C MR spectroscopy with labeled substrates, oxygen consumption rate measurements and specific inhibitors of the mitochondrial respiratory complexes, and assessed the expression of succinate dehydrogenase by Western Blot. Our results support the association between increased mitochondrial metabolism and metastatic potential, observed recently in breast cancer patients.