期刊
CANCER RESEARCH
卷 73, 期 14, 页码 4429-4438出版社
AMER ASSOC CANCER RESEARCH
DOI: 10.1158/0008-5472.CAN-13-0080
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资金
- German Research Foundation (DFG) [FE1185]
- NIH [5-P50-090381-09, 5-P30-CA14051-39, 1R01DK075850-01, 1R01CA160458-01A1]
- Glenn Foundation for Medical Research
- LAM Foundation
- Burrough's Wellcome Fund
- Smith Family
- Damon Runyon Cancer Research Foundation
Metformin inhibits cancer cell proliferation, and epidemiology studies suggest an association with increased survival in patients with cancer taking metformin; however, the mechanism by which metformin improves cancer outcomes remains controversial. To explore how metformin might directly affect cancer cells, we analyzed how metformin altered the metabolism of prostate cancer cells and tumors. We found that metformin decreased glucose oxidation and increased dependency on reductive glutamine metabolism in both cancer cell lines and in a mouse model of prostate cancer. Inhibition of glutamine anaplerosis in the presence of metformin further attenuated proliferation, whereas increasing glutamine metabolism rescued the proliferative defect induced by metformin. These data suggest that interfering with glutamine may synergize with metformin to improve outcomes in patients with prostate cancer. (C) 2013 AACR.
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