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Glucose transporter 3 performs a critical role in mTOR-mediated oncogenic glycolysis and tumorigenesis

Yanbin Zhang1, Can Wei1, Junhua Xi2

  • 1Department of Urology, The First Affiliated Hospital of Anhui Medical University, Hefei, Anhui 230032, P.R. China ; Department of Urology, Hefei Hospital Affiliated to Anhui Medical University and The Second People's Hospital of Hefei, Hefei, Anhui 230011, P.R. China.

Oncology Letters
|July 3, 2015
PubMed

Insights

Mammalian target of rapamycin (mTOR) controls glucose transporter 3 (Glut3) expression, impacting cancer glycolysis and tumor growth. Downregulating Glut3 reduces tumor formation in mTOR-activated cells, identifying Glut3 as a potential therapeutic target.

Area of Science:

  • Biochemistry
  • Oncology
  • Cell Biology

Background:

  • The mammalian target of rapamycin (mTOR) pathway is frequently dysregulated in cancer, promoting oncogenic glycolysis.
  • Glucose transporter 3 (Glut3) is crucial for glucose uptake in cancer cells.
  • The precise relationship between mTOR signaling and Glut3 in tumorigenesis remains incompletely understood.

Purpose of the Study:

  • To investigate the role of Glut3 as a downstream target of mTOR in oncogenic glycolysis and tumorigenesis.
  • To elucidate the regulatory mechanism of Glut3 expression by mTOR signaling.
  • To assess the therapeutic potential of targeting Glut3 in mTOR-associated cancers.

Main Methods:

  • Western blot and quantitative PCR to compare Glut3 expression in Tsc2-deficient and wild-type mouse embryonic fibroblasts (MEFs).
  • siRNA-mediated knockdown of Glut3 to assess its effect on glycolytic rate in Tsc2-/- MEFs.
  • In vivo tumor formation assays using nude mice injected with MEFs with altered Glut3 expression.

Main Results:

  • Glut3 expression is upregulated by mTOR in Tsc2-/- MEFs.
  • Downregulation of Glut3 significantly reduced the glycolytic rate in Tsc2-/- cells.
  • Reduced Glut3 expression diminished tumor formation in vivo in a model of hyperactive mTORC1 signaling.

Conclusions:

  • Glut3 is a novel downstream target of mTOR complex 1 (mTORC1).
  • Glut3 plays a critical role in mTORC1-driven oncogenic glycolysis and tumorigenesis.
  • Targeting Glut3 represents a promising therapeutic strategy for cancers with dysregulated mTORC1 signaling.
Keywords:
Glut3glycolysismTORtumorigenesis

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