Evaluation of 2-deoxy-D-glucose as a chemotherapeutic agent: mechanism of cell death

Br J Cancer. 2002 Sep 23;87(7):805-12. doi: 10.1038/sj.bjc.6600547.

Abstract

Nutrient deprivation has been shown to cause cancer cell death. To exploit nutrient deprivation as anti-cancer therapy, we investigated the effects of the anti-metabolite 2-deoxy-D-glucose on breast cancer cells in vitro. This compound has been shown to inhibit glucose metabolism. Treatment of human breast cancer cell lines with 2-deoxy-D-glucose results in cessation of cell growth in a dose dependent manner. Cell viability as measured by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide conversion assay and clonogenic survival are decreased with 2-deoxy-D-glucose treatment indicating that 2-deoxy-D-glucose causes breast cancer cell death. The cell death induced by 2-deoxy-D-glucose was found to be due to apoptosis as demonstrated by induction of caspase 3 activity and cleavage of poly (ADP-ribose) polymerase. Breast cancer cells treated with 2-deoxy-D-glucose express higher levels of Glut1 transporter protein as measured by Western blot analysis and have increased glucose uptake compared to non-treated breast cancer cells. From these results we conclude that 2-deoxy-D-glucose treatment causes death in human breast cancer cell lines by the activation of the apoptotic pathway. Our data suggest that breast cancer cells treated with 2-deoxy-D-glucose accelerate their own demise by initially expressing high levels of glucose transporter protein, which allows increased uptake of 2-deoxy-D-glucose, and subsequent induction of cell death. These data support the targeting of glucose metabolism as a site for chemotherapeutic intervention by agents such as 2-deoxy-D-glucose.

MeSH terms

  • Antineoplastic Agents / pharmacology*
  • Apoptosis / drug effects*
  • Biological Transport / drug effects
  • Breast Neoplasms / drug therapy
  • Caspase 3
  • Caspases / metabolism
  • Cell Division / drug effects
  • Cell Survival / drug effects
  • Deoxyglucose / pharmacology*
  • Drug Design
  • Glucose / metabolism
  • Glucose Transporter Type 1
  • Humans
  • Monosaccharide Transport Proteins / metabolism
  • Poly(ADP-ribose) Polymerases / metabolism
  • Time Factors
  • Tumor Cells, Cultured

Substances

  • Antineoplastic Agents
  • Glucose Transporter Type 1
  • Monosaccharide Transport Proteins
  • SLC2A1 protein, human
  • Deoxyglucose
  • Poly(ADP-ribose) Polymerases
  • CASP3 protein, human
  • Caspase 3
  • Caspases
  • Glucose