Journal
CELL REPORTS
Volume 24, Issue 9, Pages 2381-+Publisher
CELL PRESS
DOI: 10.1016/j.celrep.2018.07.086
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Funding
- Canadian Cancer Society Research Institute (CCSRI)
- Canadian Institutes of Health Research (CIHR)
- Terry Fox Research Institute (TFRI)
- Beatrice Hunter Cancer Research Institute (BHCRI)
- CIHR
- NIH/NIDDK [K01 DK098285]
- Dalhousie Medical Research Foundation (DMRF)
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [K01DK098285] Funding Source: NIH RePORTER
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NAD(+) is a key metabolic redox cofactor that is regenerated from nicotinamide through the NAD(+) salvage pathway. Here, we find that inhibiting the NAD(+) salvage pathway depletes serine biosynthesis from glucose by impeding the NAD(+)-dependent protein, 3-phosphoglycerate dehydrogenase (PHGDH). Importantly, we find that PHGDH(high) breast cancer cell lines are exquisitely sensitive to inhibition of the NAD(+) salvage pathway. Further, we find that PHGDH protein levels and those of the rate-limiting enzyme of NAD(+) salvage, NAMPT, correlate in ER-negative, basal-like breast cancers. Although NAD(+) salvage pathway inhibitors are actively being pursued in cancer treatment, their efficacy has been poor, and our findings suggest that they may be effective for PHGDH-dependent cancers.
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