Farnesyltransferase inhibitors: antineoplastic mechanism and clinical prospects

Curr Opin Cell Biol. 2000 Apr;12(2):166-73. doi: 10.1016/s0955-0674(99)00072-1.


Recent work suggests that farnesyltransferase inhibitors suppress cancer cell proliferation through mechanisms other than inhibiting Ras isoprenylation, which is not a crucial event. Recent evidence also suggests that the antineoplastic properties of farnesyltransferase inhibitors are due to alterations in the isoprenylation of RhoB, an endosomal Rho protein that functions in receptor trafficking. A shift in conceptual focus from Ras to Rho to understand how farnesyltransferase inhibitors act provides a new vantage to address old questions in the field and suggests strategies to improve and potentially widen clinical applications.

MeSH terms

  • Alkyl and Aryl Transferases / antagonists & inhibitors*
  • Animals
  • Antineoplastic Agents / pharmacology*
  • Apoptosis
  • Clinical Trials as Topic
  • Farnesyltranstransferase
  • Humans
  • Neoplasms / drug therapy*
  • Neoplasms / metabolism
  • Neoplasms / pathology
  • Protein-Serine-Threonine Kinases*
  • Proto-Oncogene Proteins / metabolism
  • Proto-Oncogene Proteins c-akt
  • ras Proteins / metabolism
  • rhoB GTP-Binding Protein / metabolism*


  • Antineoplastic Agents
  • Proto-Oncogene Proteins
  • Alkyl and Aryl Transferases
  • Farnesyltranstransferase
  • Protein-Serine-Threonine Kinases
  • Proto-Oncogene Proteins c-akt
  • ras Proteins
  • rhoB GTP-Binding Protein