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. Author manuscript; available in PMC: 2012 Jun 28.
Published in final edited form as: Cancer Biol Ther. 2010 Jun 21;9(12):1053–1056. doi: 10.4161/cbt.9.12.12451

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.