ATF4-dependent fructolysis fuels growth of glioblastoma multiforme

Chao Chen, Zhenxing Zhang, Caiyun Liu, Bin Wang, Ping Liu, Shu Fang, Fan Yang, Yongping You and Xinjian Li ()
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Chao Chen: Chinese Academy of Sciences
Zhenxing Zhang: Chinese Academy of Sciences
Caiyun Liu: Chinese Academy of Sciences
Bin Wang: Chinese Academy of Sciences
Ping Liu: Chinese Academy of Sciences
Shu Fang: Chinese Academy of Sciences
Fan Yang: Chinese Academy of Sciences
Yongping You: The First Affiliated Hospital of Nanjing Medical University
Xinjian Li: Chinese Academy of Sciences

Nature Communications, 2022, vol. 13, issue 1, 1-13

Abstract: Abstract Excessive consumption of fructose in the Western diet contributes to cancer development. However, it is still unclear how cancer cells coordinate glucose and fructose metabolism during tumor malignant progression. We demonstrate here that glioblastoma multiforme (GBM) cells switch their energy supply from glycolysis to fructolysis in response to glucose deprivation. Mechanistically, glucose deprivation induces expression of two essential fructolytic proteins GLUT5 and ALDOB through selectively activating translation of activating transcription factor 4 (ATF4). Functionally, genetic or pharmacological disruption of ATF4-dependent fructolysis significantly inhibits growth and colony formation of GBM cells in vitro and GBM growth in vivo. In addition, ATF4, GLUT5, and ALDOB levels positively correlate with each other in GBM specimens and are poor prognostic indicators in GBM patients. This work highlights ATF4-dependent fructolysis as a metabolic feature and a potential therapeutic target for GBM.

Date: 2022
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DOI: 10.1038/s41467-022-33859-9

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