Toxin from Cobra Venom Shrinks Lung Tumors in Mouse Model

Cancer researchers have found that treating a mouse model of human lung cancer with alpha-cobratoxin blocked nicotine receptors on the lung cancer cells, which caused the tumors to shrink and prolonged the animals' lives.

Alpha-cobratoxin (alpha-CbT) is a component of the venom of certain Naja cobras. It is a muscle-type nicotinic acetylcholine receptor (nAChR) antagonist, which causes paralysis by preventing the binding of acetylcholine to the nAChR. Alpha-CbT consists of 71 amino acid residues and 5 disulfide bridges.

Investigators from the Italian National Cancer Research Institute (Genoa, Italy) grafted human non-small-cell lung carcinoma (NSCLC) onto the lungs of a group of immunocompromised mice. After the tumors had become well established, the mice were separated into three groups that were treated either with cisplatin - the standard chemotherapy drug, alpha-CbT, or a placebo.

Results published in the June 15, 2009, issue of the American Journal of Respiratory and Critical Care Medicine revealed that the mice treated with cisplatin had 16% longer median survival time than untreated mice. The animals treated with alpha-CbT had an increased median survival time of 1.7 times greater than the cisplatin-treated group and 2.1 times greater than the placebo group. Alpha-CbT appeared to be nontoxic to non-cancerous cells.

"The results of this study show that alpha-CbT, a powerful, high-affinity nAChR inhibitor, induces antitumor activity against NSCLC by triggering apoptosis,” explained contributing author Dr. Patrizia Russo, a researcher in the lung cancer unit of the National Cancer Research Institute. "The goal of this research line is to explore the widest range of possibilities of intervention on the nAChRs. We hope to move further on towards the clinical setting experimentation phase for the assessment of potentially new treatment strategies for NSCLC.”

Related Links:
National Cancer Research Institute