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ATAD2 expression increases [18F]Fluorodeoxyglucose uptake value in lung adenocarcinoma via AKT-GLUT1/HK2 pathway

  • Sun, Tong (Department of Nuclear Medicine, The first Hospital of China Medical University) ;
  • Du, Bulin (Department of Nuclear Medicine, The first Hospital of China Medical University) ;
  • Diao, Yao (Department of Nuclear Medicine, The first Hospital of China Medical University) ;
  • Li, Xuena (Department of Nuclear Medicine, The first Hospital of China Medical University) ;
  • Chen, Song (Department of Nuclear Medicine, The first Hospital of China Medical University) ;
  • Li, Yaming (Department of Nuclear Medicine, The first Hospital of China Medical University)
  • Received : 2019.02.11
  • Accepted : 2019.05.13
  • Published : 2019.07.31

Abstract

[18F]Fluorodeoxyglucose (FDG) PET/CT imaging has been widely used in the diagnosis of malignant tumors. ATPase family AAA domain-containing protein 2 (ATAD2) plays important roles in tumor growth, invasion and metastasis. However, the relationship between [18F]FDG accumulation and ATAD2 expression remains largely unknown. This study aimed to investigate the correlation between ATAD2 expression and [18F]FDG uptake in lung adenocarcinoma (LUAD), and elucidate its underlying molecular mechanisms. The results showed that ATAD2 expression was positively correlated with maximum standardized uptake value ($SUV_{max}$), total lesion glycolysis (TLG), glucose transporter type 1 (GLUT1) expression and hexokinase2 (HK2) expression in LUAD tissues. In addition, ATAD2 knockdown significantly inhibited the proliferation, tumorigenicity, migration, [18F]FDG uptake and lactate production of LUAD cells, while, ATAD2 overexpression exhibited the opposite effects. Furthermore, ATAD2 modulated the glycometabolism of LUAD via AKT-GLUT1/HK2 pathway, as assessed using LY294002 (an inhibitor of PI3K/AKT pathway). In summary, to explore the correlation between ATAD2 expression and glycometabolism is expected to bring good news for anti-energy metabolism therapy of cancers.

Keywords

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