2. Academic Validation
  3. ATF4-dependent fructolysis fuels growth of glioblastoma multiforme

ATF4-dependent fructolysis fuels growth of glioblastoma multiforme

  • Nat Commun. 2022 Oct 16;13(1):6108. doi: 10.1038/s41467-022-33859-9.
Chao Chen # 1,  Zhenxing Zhang # 1,  Caiyun Liu 1 2,  Bin Wang 1 2,  Ping Liu 1,  Shu Fang 1 2,  Fan Yang 1 2,  Yongping You 3 4,  Xinjian Li 5 6
Affiliations

Affiliations

  • 1 CAS Key Laboratory of Infection and Immunity, CAS Center for Excellence in Biomacromolecules, Institute of Biophysics, Chinese Academy of Sciences, Beijing, 100101, China.
  • 2 College of Life Sciences, University of Chinese Academy of Sciences, Beijing, 100049, China.
  • 3 Department of Neurosurgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing, 210029, China.
  • 4 Institute for Brain Tumors, Jiangsu Key Lab of Cancer Biomarkers, Prevention and Treatment, Jiangsu Collaborative Innovation Center for Cancer Personalized Medicine, Nanjing Medical University, Nanjing, 211166, China.
  • 5 CAS Key Laboratory of Infection and Immunity, CAS Center for Excellence in Biomacromolecules, Institute of Biophysics, Chinese Academy of Sciences, Beijing, 100101, China. lixinjian@ibp.ac.cn.
  • 6 College of Life Sciences, University of Chinese Academy of Sciences, Beijing, 100049, China. lixinjian@ibp.ac.cn.
  • # Contributed equally.
PMID: 36245009 DOI: 10.1038/s41467-022-33859-9
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.

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