Mechanism of action of tubulysin, an antimitotic peptide from myxobacteria

Chembiochem. 2006 Apr;7(4):678-83. doi: 10.1002/cbic.200500421.

Abstract

Tubulysin A is a highly cytotoxic peptide with antimitotic activity that induces depletion of cell microtubules and triggers the apoptotic process. Treated cells accumulated in the G2/M phase. Tubulysin A inhibited tubulin polymerization more efficiently than vinblastine and induced depolymerization of isolated microtubule preparations. Microtubule depolymerization could not be prevented by preincubation with epothilone B and paclitaxel, neither in cell-free systems nor in cell lines. In competition experiments, tubulysin A strongly interfered with the binding of vinblastine to tubulin in a noncompetitive way; the apparent Ki was 3 microM. Electron microscopy investigations showed that tubulysin A induced the formation of rings, double rings, and pinwheel structures. The mode of action of tubulysin A resembled that of peptide antimitotics dolastatin 10, phomopsin A, and hemiasterlin. Efforts are underway to develop this new group of compounds as anticancer drugs.

MeSH terms

  • Antineoplastic Agents / chemistry
  • Antineoplastic Agents / pharmacology*
  • Binding Sites
  • Binding, Competitive
  • Cell Cycle / drug effects
  • Cells, Cultured
  • Drug Screening Assays, Antitumor
  • Humans
  • Microscopy, Electron
  • Molecular Conformation
  • Myxococcales / chemistry*
  • Oligopeptides / chemistry
  • Oligopeptides / pharmacology*
  • Sensitivity and Specificity
  • Structure-Activity Relationship
  • Time Factors

Substances

  • Antineoplastic Agents
  • Oligopeptides
  • tubulysin A