The metabolic function of cyclin D3–CDK6 kinase in cancer cell survival

Haizhen Wang, Brandon N. Nicolay, Joel M. Chick, Xueliang Gao, Yan Geng, Hong Ren, Hui Gao, Guizhi Yang, Juliet A. Williams, Jan M. Suski, Mark A. Keibler, Ewa Sicinska, Ulrike Gerdemann, W. Nicholas Haining, Thomas M. Roberts, Kornelia Polyak, Steven P. Gygi, Nicholas J. Dyson and Piotr Sicinski ()
Additional contact information
Haizhen Wang: Dana-Farber Cancer Institute
Brandon N. Nicolay: Massachusetts General Hospital Cancer Center
Joel M. Chick: Harvard Medical School
Xueliang Gao: Dana-Farber Cancer Institute
Yan Geng: Dana-Farber Cancer Institute
Hong Ren: Dana-Farber Cancer Institute
Hui Gao: Novartis Institutes for Biomedical Research
Guizhi Yang: Novartis Institutes for Biomedical Research
Juliet A. Williams: Novartis Institutes for Biomedical Research
Jan M. Suski: Dana-Farber Cancer Institute
Mark A. Keibler: Massachusetts Institute of Technology
Ewa Sicinska: Dana-Farber Cancer Institute
Ulrike Gerdemann: Dana-Farber Cancer Institute
W. Nicholas Haining: Dana-Farber Cancer Institute
Thomas M. Roberts: Dana-Farber Cancer Institute
Kornelia Polyak: Dana-Farber Cancer Institute
Steven P. Gygi: Harvard Medical School
Nicholas J. Dyson: Massachusetts General Hospital Cancer Center
Piotr Sicinski: Dana-Farber Cancer Institute

Nature, 2017, vol. 546, issue 7658, 426-430

Abstract: The cyclin D3–CDK6 kinase complex, which is overactive in some cancers, inhibits two key glycolysis enzymes and thereby enhances the levels of antioxidants in cells, promoting tumour cell survival.

Date: 2017
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DOI: 10.1038/nature22797

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