The use of high-content screening for the discovery and characterization of compounds that modulate mitotic index and cell cycle progression by differing mechanisms of action

Assay Drug Dev Technol. 2006 Apr;4(2):153-63. doi: 10.1089/adt.2006.4.153.

Abstract

The advent of high-content screening has expanded the ability of researchers to identify and quantify compound effects on a number of cellular events in a manner that allows for the rapid screening of chemical libraries. We have validated an approach for characterizing inhibitors of Aurora kinase family members using high-content screening by determining compound effects on the levels of the mitotic marker phospho-histone H3 (Ser10). Analysis of the data from these experiments led us to the discovery of a series of related compounds that increased the level of cells staining positive for the mitotic marker, indicating a block of cell cycle progression at M-phase. We then reconfigured the Aurora kinase inhibition assay and validated a high-content approach to identify compounds that block progression through M-phase. We were able to take advantage of the flexibility within the high-content screening platform to measure DNA content, activation of apoptosis, and effects on beta-tubulin staining patterns, all of which directly led to the identification of the cellular target of this new class of compounds.

MeSH terms

  • Antineoplastic Agents / pharmacology*
  • Apoptosis / drug effects
  • Aurora Kinases
  • Biological Assay / methods*
  • Cell Cycle / drug effects*
  • Cell Cycle Proteins / antagonists & inhibitors
  • Cell Cycle Proteins / physiology
  • Cell Division / drug effects
  • Cell Line, Tumor
  • DNA, Neoplasm / analysis
  • Enzyme Inhibitors / pharmacology
  • Humans
  • Mitosis / drug effects*
  • Mitotic Index / methods*
  • Protein Serine-Threonine Kinases / antagonists & inhibitors
  • Protein Serine-Threonine Kinases / metabolism
  • Tubulin / metabolism

Substances

  • Antineoplastic Agents
  • Cell Cycle Proteins
  • DNA, Neoplasm
  • Enzyme Inhibitors
  • Tubulin
  • Aurora Kinases
  • Protein Serine-Threonine Kinases