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Nicotine exerts its oncogenic effects through the binding to nicotinic acetylcholine receptors (nAChRs) and the activation of downstream pathways that block apoptosis and promote neo-angiogenesis. The nAChRs of the α7 subtype are present on a wide variety of cancer cells and their inhibition by cobra venom neurotoxins has been proposed in several articles and reviews as a potential innovative lung cancer therapy. However, since part of the published results was recently retracted, we believe that the antitumoral activity of cobra venom neurotoxins needs to be independently re-evaluated.  We determined the activity of α-neurotoxins from  Naja atra  (short-chain neurotoxin, α-cobrotoxin) and  Naja kaouthia  (long-chain neurotoxin, α-cobratoxin)  in vitro  by cytotoxicity measurements in 5 lung cancer cell lines, by colony formation assay with α7nAChRs expressing and non-expressing cell lines and  in vivo  by assessing tumor growth in an orthotopic Non-Obese Diabetic/Severe Combined Immunodeficient ( NOD/SCID ) mouse model system utilizing different treatment schedules and dosages.  No statistically significant reduction in tumor growth was observed in the treatment arms in comparison to the control for both toxins. Paradoxically α-cobrotoxin from  Naja atra  showed the tendency to enhance tumor growth although, even in this case, the statistical significance was not reached.  In conclusion our results show that, in contrast with other reports, the nAChR inhibitors α-cobratoxin from  N. kaouthia  and α-cobrotoxin from  N. atra  neither suppressed tumor growth nor prolonged the survival of the treated animals.

Inhibition of the Nicotinic Acetylcholine Receptors by Cobra Venom α-Neurotoxins: Is There a Perspective in Lung Cancer Treatment?