The Guardian reported yesterday that the venom of the Brazilian wasp Polybia paulista contains a specific toxin, called MP1, that has anti-cancer properties. MP1 works by binding to certain molecules called lipids in the tumor cells' outer membranes.
When MP1 binds to the lipids, it disrupts the membrane structure and creates large holes through which molecules vital to a cancer cell’s survival leak out.
The reported research was published in
this Sept. 1, 2015 paper, entitled "PE and PS Lipids Synergystically Enhance Membrane Poration by a Peptide with Anticancer Properties".
Digression: You can think of an individual cell as a plastic bag (the outer membrane) surrounding a watery gel-like interior that contains the cell's working components. The outer membrane is not solid, like a plastic bag, however; it is composed of two layers of fatty molecules called lipids that arrange themselves tail-to-tail to form the outer boundary of the cell. Proteins can thus be easily inserted into the membrane; for example, natural killer cells in your body kill cells by secreting a protein called perforin, which embed into the membrane of a cell to be killed and literally "perforate" it, allowing the contents to leak out, and more importantly, water to leak in - too much water, and the cell bursts.
Turning back to the wasp and MP1, the really intriguing aspect is that
laboratory tests suggested that the molecule was harmless to healthy cells and therefore safe, but added: “Further work would be required to prove that.”
Interestingly, the anticancer properties of MP1 were known
back in 2008, as reported in a paper by Wang et al. out of Lanzhou University (China). The abstract to the linked article concludes "polybia-MPI may offer a novel therapeutic strategy in the treatment of prostate cancer and bladder cancer, considering its relatively lower cytoxicity to normal cells." The same group
in 2009 suggested that the mode of action of MP1 was at the cell surface, not within the cell.
Moreover, a group in Brazil, headed by Mario Sergio Palma (one of the authors of the 2015 paper, above) reported in 2012 that MP1, which is actually a small protein, not only influenced the cell's membrane, but was more toxic to leukemic T cells than to normal T cells. They also found, surprisingly, that one reason for this difference in MP1's effects is that lukemia cells have less cholesterol in the cell membrane than do healthy cells!
So by September 1, 2015, a lot was already known about MP1, its structure, its mode of action against cells, and its anti-cancer activity. What did the authors of the 2015 article bring to the table? They found that two cell membrane lipids, PS (phosphatidyl serine) and PE (phosphatidylethanolamine), which are apparently enriched in tumor cells outer membranes, synergistically acted to make the tumor cells more susceptible to membrane poration by MP1.
So, rather than being a ground-breaking new stride in cancer research, the 2015 paper is, as most scientific papers are, a report of a new understanding to a known system. This is not to disparage the paper, however; this is the way scientific understanding progresses, and "breakthroughs" are more often than not the result of an accretion of new understandings that makes, in this case, new anti-cancer therapies more possible.
(PS - So if so much was known about MP1 before, why the excitement now? I think it's because Cell Press, which runs Biophysical Journal, the journal in which the 2015 results were published, put out a press release. A little marketing never hurts.)