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Comment
. 2010 Jun 15;9(12):1053-6.
doi: 10.4161/cbt.9.12.12451. Epub 2010 Jun 21.

Voltage dependent anion channel-1 (VDAC-1) as an anti-cancer target

Saroj P Mathupala  1 , Peter L Pedersen
Affiliations
Free PMC article
Comment

Voltage dependent anion channel-1 (VDAC-1) as an anti-cancer target

Saroj P Mathupala et al. Cancer Biol Ther. .
Free PMC article
No abstract available

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Figure 1
Figure 1
Silencing of VDAC-1 expression via RNAi may result in opposing physiological effects on the tumor cell. Dispossessing of an “anchor” for hexokinase on the outer mitochondrial membrane may deprive the tumor of a high flux rate of glycolysis, thus inhibiting tumor proliferation; Pro-apoptotic—the same can relieve the anti-apoptotic effects that result from the hexokinase-VDAC interaction. Anti-apoptotic—if oligomers of VDAC are involved in forming the mitochondrial permeability transition pore complex (MPTP), silencing VDAC may inhibit apoptosis; the same may occur if VDAC is involved in hetero-multimer formation with Bax or other pro-apoptotic members of the Bcl-2 family of proteins. Despite the opposing effects on apoptosis, the data presented by Koren et al. indicate that silencing VDAC-1 inhibits tumor metabolism significantly, most likely via disruption of both the enhanced glycolytic flux and the nucleotide/metabolite/ion shuttles across mitochondria.
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