Background: VDAC (Voltage-Dependent Anion selective Channel) is a small
family of abundant pore-forming proteins located in the outer mitochondrial membrane. Their
role range from the most intuitive, the formation of a hydrophilic conduit through the membrane
thanks to its beta-barrel structure, to less understood functions that make them essential
actors in the cross-talk between the bioenergetics metabolism and the cytosol components.
Due to this localization, VDAC1, in particular, has been reported to be involved in apoptosis,
Hexokinase and tubulin binding, and in the Warburg effect. For these reasons, an involvement
of VDAC in cancer is considered consequential and a number of compounds have been proposed
and used in experimental trials to demonstrate the efficacy of molecules affecting the
functions of VDAC.
Objectives: In this work, we thus survey the literature describing drug compounds acting on
the cancerous proliferation through VDAC. Three main categories have been assigned: molecules
acting on the VDAC-Hexokinase binding, molecules directly inhibiting the VDAC conductance,
molecules affecting the expression levels of the VDAC gene. The application of
biological peptides for this purpose is also considered.
Conclusion: Since the knowledges about the functional properties of VDAC protein are still
insufficient, VDAC as a pharmacological target in the fight against cancer is still a very open,
but very promising, field.