Vipers are efficient killers but a protein in their venom has been found to prevent the spread of tumours in laboratory mice. Researchers are now developing a molecular "portrait" of the protein to help explain how it works.
The study, by Dr Mary Ann McLane of the University of Delaware, and Dr Stefan Niewia rowski of Temple University, Philadelphia, is published in the current issue of Cardiology Today. Venom from Macmahon's viper (Eristocophis macmahoni) found in Afghanistan and Pakistan, contains the protein, eristostatin. This substance blocks the metastasis or spread of tumours in mice injected with cancer cells, according to Dr McLane.
This blocking action has been recognised since 1995. A Canadian researcher, Dr Vincent L Morris, of the University of Western Ontario, demonstrated that cancer-susceptible mice injected with melanoma cells had significantly less active cancer growth if they also received the eristostatin protein.
The new work is an attempt to better understand the structure of this protein because structure is a major factor in how a protein does its job. "The next step is to find out exactly what it is about the structure of eristostatin that gives it this exciting capability in mice," Dr McLane said.
Eristostatin is one of many known viper venom "disinte grins", proteins that interact with the biochemical hooks on cells which are known as receptors. Disintegrins in particular inhibit blood clotting by stopping the reaction between fibrinogen and platelets, the main building blocks of blood clots.
The study of the protein has already led to the development of an anti-platelet drug, but work on understanding its anti-tumour effect is just beginning. Dr McLane's work has focused on a protruding section of the protein - the RGD loop - which plays a role in binding with the cell receptor. Learning about the structure could assist pharmaceutical companies to develop cancer drugs, according to the researchers.