Significance

Serine supports a number of anabolic processes, including protein, lipid, and nucleic acid synthesis. Cells can either import serine or synthesize it de novo. Recently, overexpression of 3-phosphoglycerate dehydrogenase (PHGDH), the gene encoding the first committed step of serine synthesis, via focal amplification and other mechanisms, has been identified in human cancers. Cancer cell lines that overexpress PHGDH are uniquely sensitive to PHGDH knockdown whereas lines that express little PHGDH are insensitive, suggesting that PHGDH may be a clinically interesting target. Here, we report the discovery of a specific small molecule inhibitor of PHGDH, which enables preclinical evaluation of PHGDH as a target in cancer and provides a tool to study the biology of de novo serine synthesis.

Abstract

Cancer cells reprogram their metabolism to promote growth and proliferation. The genetic evidence pointing to the importance of the amino acid serine in tumorigenesis is striking. The gene encoding the enzyme 3-phosphoglycerate dehydrogenase (PHGDH), which catalyzes the first committed step of serine biosynthesis, is overexpressed in tumors and cancer cell lines via focal amplification and nuclear factor erythroid-2-related factor 2 (NRF2)-mediated up-regulation. PHGDH-overexpressing cells are exquisitely sensitive to genetic ablation of the pathway. Here, we report the discovery of a selective small molecule inhibitor of PHGDH, CBR-5884, identified by screening a library of 800,000 drug-like compounds. CBR-5884 inhibited de novo serine synthesis in cancer cells and was selectively toxic to cancer cell lines with high serine biosynthetic activity. Biochemical characterization of the inhibitor revealed that it was a noncompetitive inhibitor that showed a time-dependent onset of inhibition and disrupted the oligomerization state of PHGDH. The identification of a small molecule inhibitor of PHGDH not only enables thorough preclinical evaluation of PHGDH as a target in cancers, but also provides a tool with which to study serine metabolism.

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Acknowledgments

We thank U. Oppermann, M. G. Vander Heiden, K. R. Mattaini, and M. Yuan for technical assistance and reagents. We thank J. Johnson, Y. Zheng, H. Shim, B. D. Ngo, and other L.C.C. laboratory members for helpful discussions. L.C.C. was supported by NIH Grants P01CA117969 and P01CA120964. C.A.L. was partially supported by a PanCAN-AACR Pathway to Leadership Award and a Dale F. Frey Award for Breakthrough Scientists from the Damon Runyon Cancer Research Foundation (Grant DFS-09-14). G.M.D. was supported by a PanCAN-AACR Pathway to Leadership Award. S.-M.F. was supported by a Conquer Cancer Now Award from the Concern Foundation.

Supporting Information

Supporting Information (PDF)
Supporting Information
pnas.1521548113.st01.xlsx

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Information & Authors

Information

Published in

The cover image for PNAS Vol.113; No.7
Proceedings of the National Academy of Sciences
Vol. 113 | No. 7
February 16, 2016
PubMed: 26831078

Classifications

Submission history

Published online: February 1, 2016
Published in issue: February 16, 2016

Keywords

  1. PHGDH
  2. inhibitor
  3. serine
  4. cancer metabolism

Acknowledgments

We thank U. Oppermann, M. G. Vander Heiden, K. R. Mattaini, and M. Yuan for technical assistance and reagents. We thank J. Johnson, Y. Zheng, H. Shim, B. D. Ngo, and other L.C.C. laboratory members for helpful discussions. L.C.C. was supported by NIH Grants P01CA117969 and P01CA120964. C.A.L. was partially supported by a PanCAN-AACR Pathway to Leadership Award and a Dale F. Frey Award for Breakthrough Scientists from the Damon Runyon Cancer Research Foundation (Grant DFS-09-14). G.M.D. was supported by a PanCAN-AACR Pathway to Leadership Award. S.-M.F. was supported by a Conquer Cancer Now Award from the Concern Foundation.

Authors

Affiliations

Edouard Mullarky
Meyer Cancer Center, Weill Cornell Medical College, New York, NY 10065;
Department of Medicine, Weill Cornell Medical College, New York, NY 10065;
Biological and Biomedical Sciences Graduate Program, Harvard Medical School, Boston, MA 02115;
Natasha C. Lucki
The California Institute for Biomedical Research, La Jolla, CA 92037;
Reza Beheshti Zavareh
The California Institute for Biomedical Research, La Jolla, CA 92037;
Justin L. Anglin
The California Institute for Biomedical Research, La Jolla, CA 92037;
Ana P. Gomes
Meyer Cancer Center, Weill Cornell Medical College, New York, NY 10065;
Department of Pharmacology, Weill Cornell Medical College, New York, NY 10065;
Brandon N. Nicolay
Massachusetts General Hospital Cancer Center, Harvard Medical School, Charlestown, MA 02129;
Jenny C. Y. Wong
Meyer Cancer Center, Weill Cornell Medical College, New York, NY 10065;
Department of Medicine, Weill Cornell Medical College, New York, NY 10065;
Stefan Christen
Laboratory of Cellular Metabolism and Metabolic Regulation, Department of Oncology, Katholieke Universiteit Leuven, 3000 Leuven, Belgium;
Laboratory of Cellular Metabolism and Metabolic Regulation, Vesalius Research Center, Vlaams Instituut voor Biotechnologie Leuven, 3000 Leuven, Belgium;
Hidenori Takahashi
Department of Systems Biology, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA 02115;
Division of Signal Transduction, Department of Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA 02115;
Present address: Frontier Research Laboratories, Daiichi Sankyo Co., Shinagawa-ku, Tokyo 140-8710, Japan.
Pradeep K. Singh
Department of Biochemistry, Weill Cornell Medical College, New York, NY 10065;
Milstein Chemistry Core Facility, Weill Cornell Medical College, New York, NY 10065;
John Blenis
Meyer Cancer Center, Weill Cornell Medical College, New York, NY 10065;
Department of Pharmacology, Weill Cornell Medical College, New York, NY 10065;
Department of Biochemistry, Weill Cornell Medical College, New York, NY 10065;
Milstein Chemistry Core Facility, Weill Cornell Medical College, New York, NY 10065;
Sarah-Maria Fendt
Laboratory of Cellular Metabolism and Metabolic Regulation, Department of Oncology, Katholieke Universiteit Leuven, 3000 Leuven, Belgium;
Laboratory of Cellular Metabolism and Metabolic Regulation, Vesalius Research Center, Vlaams Instituut voor Biotechnologie Leuven, 3000 Leuven, Belgium;
John M. Asara
Division of Signal Transduction, Department of Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA 02115;
Gina M. DeNicola
Meyer Cancer Center, Weill Cornell Medical College, New York, NY 10065;
Department of Medicine, Weill Cornell Medical College, New York, NY 10065;
Costas A. Lyssiotis2 [email protected]
Department of Molecular and Integrative Physiology, University of Michigan, Ann Arbor, MI 48109;
Division of Gastroenterology, Department of Internal Medicine, University of Michigan, Ann Arbor, MI 48109;
Luke L. Lairson2 [email protected]
The California Institute for Biomedical Research, La Jolla, CA 92037;
Department of Chemistry, The Scripps Research Institute, La Jolla, CA 92037
Lewis C. Cantley2 [email protected]
Meyer Cancer Center, Weill Cornell Medical College, New York, NY 10065;
Department of Medicine, Weill Cornell Medical College, New York, NY 10065;

Notes

2
To whom correspondence may be addressed. Email: [email protected], [email protected], or [email protected].
Author contributions: E.M., N.C.L., L.L.L., and L.C.C. designed research; E.M., N.C.L., R.B.Z., J.L.A., A.P.G., B.N.N., J.C.Y.W., S.C., H.T., P.K.S., J.D.W., S.-M.F., J.M.A., G.M.D., and C.A.L. performed research; E.M., N.C.L., R.B.Z., J.L.A., A.P.G., B.N.N., S.C., H.T., P.K.S., J.B., J.D.W., S.-M.F., J.M.A., G.M.D., C.A.L., L.L.L., and L.C.C. analyzed data; and E.M., C.A.L., L.L.L., and L.C.C. wrote the paper.
Reviewers: E.G., Beatson Institute for Cancer Research; and B.R.S., Columbia/Howard Hughes Medical Institute.

Competing Interests

Conflict of interest statement: L.C.C. owns equity in, receives compensation from, and serves on the Board of Directors and Scientific Advisory Board of Agios Pharmaceuticals. Agios Pharmaceuticals is identifying metabolic pathways of cancer cells and developing drugs to inhibit such enzymes to disrupt tumor cell growth and survival.

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    Identification of a small molecule inhibitor of 3-phosphoglycerate dehydrogenase to target serine biosynthesis in cancers
    Proceedings of the National Academy of Sciences
    • Vol. 113
    • No. 7
    • pp. 1673-E942

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