Peripheral benzodiazepine receptor and its clinical targeting

Anticancer Drugs. 2004 Sep;15(8):737-45. doi: 10.1097/00001813-200409000-00001.

Abstract

Tumor cell targeted therapies, by induction or enhancement of apoptosis, constitute recent promising approaches achieving more specific anti-tumor efficacy. The peripheral benzodiazepine receptor (PBR), which belongs to the permeability transition pore (PTP), the central regulatory complex of apoptosis, is a potential target. A number of findings argue in favor of the development of PBR targeting approaches: (i) overexpression of PBR has been described in a large range of human cancers, (ii) PTP-mediated regulation of programmed cell death is an apoptotic-inducing factor-independent check-point that could be modulated by various conventional cancer therapies, and (iii) PBR ligation enhances apoptosis induction in many types of tumors and reverses Bcl-2 cytoprotective effects. Altogether, these observations support the use of PBR-directed drugs, particularly PBR ligands such as Ro5-4864, in the treatment of human cancers.

Publication types

  • Review

MeSH terms

  • Animals
  • Antineoplastic Agents / pharmacology
  • Antineoplastic Agents / therapeutic use
  • Drug Delivery Systems / methods*
  • Drug Delivery Systems / trends*
  • France
  • Humans
  • Neoplasms / drug therapy
  • Neoplasms / pathology
  • Receptors, GABA-A / drug effects*
  • Receptors, GABA-A / physiology

Substances

  • Antineoplastic Agents
  • Receptors, GABA-A