Mitosis as an anti-cancer drug target

Chromosoma. 2013 Oct;122(5):431-49. doi: 10.1007/s00412-013-0419-8. Epub 2013 Jun 18.

Abstract

Suppression of cell proliferation by targeting mitosis is one potential cancer intervention. A number of existing chemotherapy drugs disrupt mitosis by targeting microtubule dynamics. While efficacious, these drugs have limitations, i.e. neuropathy, unpredictability and development of resistance. In order to overcome these issues, a great deal of effort has been spent exploring novel mitotic targets including Polo-like kinase 1, Aurora kinases, Mps1, Cenp-E and KSP/Eg5. Here we summarize the latest developments in the discovery and clinical evaluation of new mitotic drug targets.

Publication types

  • Review

MeSH terms

  • Anticarcinogenic Agents / therapeutic use*
  • Aurora Kinases / metabolism
  • Cell Cycle Proteins / metabolism
  • Cell Proliferation / drug effects
  • Chromosomal Proteins, Non-Histone / metabolism
  • Humans
  • Kinesins / metabolism
  • Mitosis / drug effects
  • Mitosis / genetics*
  • Molecular Targeted Therapy*
  • Polo-Like Kinase 1
  • Protein Serine-Threonine Kinases / metabolism
  • Protein-Tyrosine Kinases / metabolism
  • Proto-Oncogene Proteins / metabolism

Substances

  • Anticarcinogenic Agents
  • Cell Cycle Proteins
  • Chromosomal Proteins, Non-Histone
  • KIF11 protein, human
  • Proto-Oncogene Proteins
  • centromere protein E
  • Protein-Tyrosine Kinases
  • Aurora Kinases
  • Protein Serine-Threonine Kinases
  • TTK protein, human
  • Kinesins