Identification of Compounds That Decrease Glioblastoma Growth and Glucose Uptake in Vitro

ACS Chem Biol. 2018 Aug 17;13(8):2048-2057. doi: 10.1021/acschembio.8b00251. Epub 2018 Jun 15.

Abstract

Tumor heterogeneity has hampered the development of novel effective therapeutic options for aggressive cancers, including the deadly primary adult brain tumor glioblastoma (GBM). Intratumoral heterogeneity is partially attributed to the tumor initiating cell (TIC) subset that contains highly tumorigenic, stem-like cells. TICs display metabolic plasticity but can have a reliance on aerobic glycolysis. Elevated expression of GLUT1 and GLUT3 is present in many cancer types, with GLUT3 being preferentially expressed in brain TICs (BTICs) to increase survival in low nutrient tumor microenvironments, leading to tumor maintenance. Through structure-based virtual screening (SBVS), we identified potential novel GLUT inhibitors. The screening of 13 compounds identified two that preferentially inhibit the growth of GBM cells with minimal toxicity to non-neoplastic astrocytes and neurons. These compounds, SRI-37683 and SRI-37684, also inhibit glucose uptake and decrease the glycolytic capacity and glycolytic reserve capacity of GBM patient-derived xenograft (PDX) cells in glycolytic stress test assays. Our results suggest a potential new therapeutic avenue to target metabolic reprogramming for the treatment of GBM, as well as other tumor types, and the identified novel inhibitors provide an excellent starting point for further lead development.

Publication types

  • Research Support, N.I.H., Extramural

MeSH terms

  • Animals
  • Antineoplastic Agents / chemistry*
  • Antineoplastic Agents / pharmacology*
  • Astrocytes / metabolism
  • Brain Neoplasms / drug therapy*
  • Brain Neoplasms / metabolism
  • Cell Line, Tumor
  • Cell Proliferation / drug effects*
  • Cells, Cultured
  • Drug Discovery
  • Glioblastoma / drug therapy*
  • Glioblastoma / metabolism
  • Glucose / metabolism*
  • Glucose Transport Proteins, Facilitative / antagonists & inhibitors*
  • Glucose Transport Proteins, Facilitative / metabolism
  • Glycolysis / drug effects
  • Humans
  • Mice
  • Models, Molecular
  • Neurons / drug effects
  • Neurons / metabolism
  • Small Molecule Libraries / chemistry
  • Small Molecule Libraries / pharmacology

Substances

  • Antineoplastic Agents
  • Glucose Transport Proteins, Facilitative
  • Small Molecule Libraries
  • Glucose