Disruption of the hexokinase-VDAC complex for tumor therapy Article uri icon

Overview

MeSH Major

  • Hexokinase
  • Neoplasms
  • Voltage-Dependent Anion Channels

abstract

  • Unlike mitochondria from most normal tissues, cancer cell mitochondria demonstrate an association between the glycolytic enzyme hexokinase (HK) and the voltage-dependent anion channel (VDAC). This provides a therapeutic opportunity, as the association appears to protect tumor cells from mitochondrial outer membrane permeabilization (MOMP), an event that marks the point of no return in multiple pathways leading to cell death. In this issue of Oncogene, the plant hormone methyl jasmonate (MJ) is shown to disrupt the interaction between human HK and VDAC, causing the inhibition of glycolysis and the induction of MOMP. MJ has already been shown to have selective anticancer activity in preclinical studies, and this finding may stimulate the development of a novel class of small anticancer compounds that inhibit the HK-VDAC interaction.

publication date

  • August 7, 2008

Research

keywords

  • Article

Identity

Digital Object Identifier (DOI)

  • 10.1038/onc.2008.114

Additional Document Info

start page

  • 4633

end page

  • 5

volume

  • 27

number

  • 34