Identification of cardiac glycoside molecules as inhibitors of c-Myc IRES-mediated translation

J Biomol Screen. 2013 Apr;18(4):407-19. doi: 10.1177/1087057112466698. Epub 2012 Nov 13.

Abstract

Translation initiation is a fine-tuned process that plays a critical role in tumorigenesis. The use of small molecules that modulate mRNA translation provides tool compounds to explore the mechanism of translational initiation and to further validate protein synthesis as a potential pharmaceutical target for cancer therapeutics. This report describes the development and use of a click beetle, dual luciferase cell-based assay multiplexed with a measure of compound toxicity using resazurin to evaluate the differential effect of natural products on cap-dependent or internal ribosome entry site (IRES)-mediated translation initiation and cell viability. This screen identified a series of cardiac glycosides as inhibitors of IRES-mediated translation using, in particular, the oncogene mRNA c-Myc IRES. Treatment of c-Myc-dependent cancer cells with these compounds showed a decrease in c-Myc protein associated with a significant modulation of cell viability. These findings suggest that inhibition of IRES-mediated translation initiation may be a strategy to inhibit c-Myc-driven tumorigenesis.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Apoptosis / drug effects
  • Base Sequence
  • Biological Assay
  • Cardiac Glycosides / analysis*
  • Cardiac Glycosides / chemistry
  • Cardiac Glycosides / pharmacology*
  • Cell Line, Tumor
  • Cell Proliferation / drug effects
  • Cell Survival / drug effects
  • Cymarine / chemistry
  • Cymarine / pharmacology
  • DNA Damage
  • Drug Evaluation, Preclinical*
  • Genes, Reporter
  • HEK293 Cells
  • Humans
  • Inhibitory Concentration 50
  • Protein Biosynthesis / drug effects*
  • Protein Synthesis Inhibitors / analysis
  • Protein Synthesis Inhibitors / chemistry
  • Protein Synthesis Inhibitors / pharmacology*
  • Proto-Oncogene Proteins c-myc / antagonists & inhibitors
  • Proto-Oncogene Proteins c-myc / metabolism*
  • Ribosomes / drug effects
  • Ribosomes / metabolism*
  • Vascular Endothelial Growth Factor A / metabolism

Substances

  • Cardiac Glycosides
  • Protein Synthesis Inhibitors
  • Proto-Oncogene Proteins c-myc
  • Vascular Endothelial Growth Factor A
  • Cymarine