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Disruption of the hexokinase-VDAC complex for tumor therapy

L Galluzzi1, O Kepp, N Tajeddine

  • 1INSERM, U848, 39 rue C. Desmoulins, Villejuif, France.

Oncogene
|May 13, 2008
PubMed

Insights

The plant hormone methyl jasmonate (MJ) disrupts the cancer cell hexokinase (HK)-voltage-dependent anion channel (VDAC) interaction. This inhibition of glycolysis and induction of mitochondrial outer membrane permeabilization (MOMP) offers a novel anticancer therapeutic strategy.

Area of Science:

  • Biochemistry
  • Cell Biology
  • Oncology

Background:

  • Mitochondria in cancer cells exhibit a unique association between hexokinase (HK) and voltage-dependent anion channel (VDAC).
  • This HK-VDAC interaction in tumors protects cells from mitochondrial outer membrane permeabilization (MOMP), a critical event triggering cell death pathways.

Purpose of the Study:

  • To investigate the effect of methyl jasmonate (MJ) on the HK-VDAC interaction in cancer cells.
  • To explore the potential of disrupting this interaction as an anticancer therapeutic strategy.

Main Methods:

  • Utilized biochemical assays to examine the interaction between human HK and VDAC.
  • Assessed the impact of MJ on glycolysis and MOMP induction in cancer cells.

Main Results:

  • Methyl jasmonate (MJ) was found to disrupt the association between human hexokinase (HK) and voltage-dependent anion channel (VDAC).
  • This disruption led to the inhibition of glycolysis and the subsequent induction of mitochondrial outer membrane permeabilization (MOMP).

Conclusions:

  • The plant hormone MJ effectively targets the HK-VDAC complex in cancer cells.
  • Inhibiting the HK-VDAC interaction represents a promising therapeutic avenue for developing novel anticancer agents.

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