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Influence of glucose transporter 1 activity inhibition on neuroblastoma in vitro

Yan Peng1, Si-Ning Xing1, Hu-Ying Tang1

  • 1Department of Physiology, Chongqing Medical University, Chongqing 400016, China; Department of Molecular Medicine and Cancer Research Center, Chongqing Medical University, Chongqing 400016, China.

Gene
|December 17, 2018
PubMed

Insights

The GLUT1 inhibitor WZB117 effectively reduced neuroblastoma cell viability and growth by inhibiting glycolysis. This targeted approach arrested the cell cycle and induced necrosis, suggesting GLUT1 as a promising therapeutic target for neuroblastoma.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Cancer cells exhibit high glycolysis for energy production, making glycolysis a key target for anticancer strategies.
  • Glucose transporter 1 (GLUT1) inhibitors have shown efficacy as anticancer agents.

Purpose of the Study:

  • To evaluate the effects of the selective GLUT1 inhibitor WZB117 on neuroblastoma (NB) cell line SH-SY5Y viability, cell cycle, and glycolysis in vitro.
  • To investigate WZB117 as a potential therapeutic target for NB.

Main Methods:

  • SH-SY5Y cells were treated with WZB117 and analyzed for cell viability, gene expression (qRT-PCR), protein levels (Western blot), and cell cycle progression (flow cytometry).
  • ATP and lactate dehydrogenase (LDH) levels were also measured.

Main Results:

  • WZB117 treatment significantly reduced SH-SY5Y cell viability and downregulated GLUT1 protein levels.
  • The inhibitor induced cell cycle arrest at the G0-G1 phase and promoted necrosis over apoptosis.
  • WZB117 decreased intracellular ATP, LDH, and glycolytic enzyme levels.

Conclusions:

  • WZB117-induced GLUT1 inhibition effectively suppressed neuroblastoma cell growth, induced cell cycle arrest, and reduced glycolysis metabolites in vitro.
  • GLUT1 inhibition presents a potential therapeutic strategy for neuroblastoma treatment.
Keywords:
Energy metabolismGLUT1GlycolysisNeuroblastoma

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