Polo-like kinase 1 coordinates biosynthesis during cell cycle progression by directly activating pentose phosphate pathway

Xiaoyu Ma, Lin Wang, Huang De, Yunyan Li, Dongdong Yang, Tingting Li, Fudong Li, Linchong Sun, Haoran Wei, Kun He, Fazhi Yu, Debiao Zhao, Lan Hu, Songge Xing, Zhaoji Liu, Kui Li, Jing Guo, Zhenye Yang, Xin Pan, Ailing Li, Yunyu Shi, Junfeng Wang (), Ping Gao () and Huafeng Zhang ()
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Xiaoyu Ma: CAS Key Laboratory of Innate Immunity and Chronic Disease, Innovation Center for Cell Signaling Network, School of Life Sciences, University of Science and Technology of China
Lin Wang: CAS Key Laboratory of Innate Immunity and Chronic Disease, Innovation Center for Cell Signaling Network, School of Life Sciences, University of Science and Technology of China
Huang De: CAS Key Laboratory of Innate Immunity and Chronic Disease, Innovation Center for Cell Signaling Network, School of Life Sciences, University of Science and Technology of China
Yunyan Li: Chinese Academy of Sciences
Dongdong Yang: CAS Key Laboratory of Innate Immunity and Chronic Disease, Innovation Center for Cell Signaling Network, School of Life Sciences, University of Science and Technology of China
Tingting Li: CAS Key Laboratory of Innate Immunity and Chronic Disease, Innovation Center for Cell Signaling Network, School of Life Sciences, University of Science and Technology of China
Fudong Li: University of Science and Technology of China
Linchong Sun: CAS Key Laboratory of Innate Immunity and Chronic Disease, Innovation Center for Cell Signaling Network, School of Life Sciences, University of Science and Technology of China
Haoran Wei: CAS Key Laboratory of Innate Immunity and Chronic Disease, Innovation Center for Cell Signaling Network, School of Life Sciences, University of Science and Technology of China
Kun He: National Center of Biomedical Analysis
Fazhi Yu: CAS Key Laboratory of Innate Immunity and Chronic Disease, Innovation Center for Cell Signaling Network, School of Life Sciences, University of Science and Technology of China
Debiao Zhao: University of Science and Technology of China
Lan Hu: CAS Key Laboratory of Innate Immunity and Chronic Disease, Innovation Center for Cell Signaling Network, School of Life Sciences, University of Science and Technology of China
Songge Xing: CAS Key Laboratory of Innate Immunity and Chronic Disease, Innovation Center for Cell Signaling Network, School of Life Sciences, University of Science and Technology of China
Zhaoji Liu: CAS Key Laboratory of Innate Immunity and Chronic Disease, Innovation Center for Cell Signaling Network, School of Life Sciences, University of Science and Technology of China
Kui Li: CAS Key Laboratory of Innate Immunity and Chronic Disease, Innovation Center for Cell Signaling Network, School of Life Sciences, University of Science and Technology of China
Jing Guo: CAS Key Laboratory of Innate Immunity and Chronic Disease, Innovation Center for Cell Signaling Network, School of Life Sciences, University of Science and Technology of China
Zhenye Yang: CAS Key Laboratory of Innate Immunity and Chronic Disease, Innovation Center for Cell Signaling Network, School of Life Sciences, University of Science and Technology of China
Xin Pan: National Center of Biomedical Analysis
Ailing Li: National Center of Biomedical Analysis
Yunyu Shi: University of Science and Technology of China
Junfeng Wang: Chinese Academy of Sciences
Ping Gao: CAS Key Laboratory of Innate Immunity and Chronic Disease, Innovation Center for Cell Signaling Network, School of Life Sciences, University of Science and Technology of China
Huafeng Zhang: CAS Key Laboratory of Innate Immunity and Chronic Disease, Innovation Center for Cell Signaling Network, School of Life Sciences, University of Science and Technology of China

Nature Communications, 2017, vol. 8, issue 1, 1-15

Abstract: Abstract Two hallmarks for cancer cells are the accelerated cell cycle progression as well as the altered metabolism, however, how these changes are coordinated to optimize the growth advantage for cancer cells are still poorly understood. Here we identify that Polo-like kinase 1 (Plk1), a key regulator for cell mitosis, plays a critical role for biosynthesis in cancer cells through activating pentose phosphate pathway (PPP). We find that Plk1 interacts with and directly phosphorylates glucose-6-phosphate dehydrogenase (G6PD). By activating G6PD through promoting the formation of its active dimer, Plk1 increases PPP flux and directs glucose to the synthesis of macromolecules. Importantly, we further demonstrate that Plk1-mediated activation of G6PD is critical for its role to promote cell cycle progression and cancer cell growth. Collectively, these findings establish a critical role for Plk1 in regulating biosynthesis in cancer cells, exemplifying how cell cycle progression and metabolic reprogramming are coordinated for cancer progression.

Date: 2017
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DOI: 10.1038/s41467-017-01647-5

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