M1 Research Paper
What is the claim?
A possible cure for certain types of cancer.
The social wasp Polybia paulista protects itself against predators by producing venom known to contain a powerful cancer-fighting ingredient. A study published this month reveals exactly how the venom's toxin called MP1 (Polybia-MP1) selectively kills cancer cells without harming normal cells. MP1 interacts with lipids that are abnormally distributed on the surface of cancer cells, creating gaping holes that allow molecules crucial for cell function to leak out.
A cancer therapy that could damage the lipid composition of a cell membrane would be a new chapter in finding an anticancer drug. It could be the start in developing new combination therapies, where multiple drugs are used …show more content…
MP1 acts against microbial pathogens by disrupting the bacterial cell membrane. The antimicrobial peptide shows promise for protecting humans from cancer as it can inhibit the growth of prostate and bladder cancer cells, as well as multi-drug resistant leukemic cells. However, it was unclear how MP1 selectively destroys cancer cells without harming normal cells.
Researchers Beales and João Ruggiero Neto from the São Paulo State University in Brazil suspected that the reason might have something to do with the unique properties of cancer cell membranes. In healthy cell membranes, phospholipids called phosphatidylserine (PS) and phosphatidylethanolamine (PE) are located in the inner membrane leaflet facing the inside of the cell. But in cancer cells, PS and PE are embedded in the outer membrane leaflet facing the cell surroundings.
How was the research tested?
The researchers tested their theory by creating model membranes, some of which contained PE and/or PS, and exposing them to MP1. They used a wide range of imaging and biophysical techniques to characterize MP1's destructive effects on the membranes. Strikingly, the presence of PS increased the binding of MP1 to the membrane by a factor of 7 to 8. On the other hand, the presence of PE enhanced MP1's ability to quickly disrupt the membrane, increasing the size of holes by a factor of 20 to
A possible cure for certain types of cancer.
The social wasp Polybia paulista protects itself against predators by producing venom known to contain a powerful cancer-fighting ingredient. A study published this month reveals exactly how the venom's toxin called MP1 (Polybia-MP1) selectively kills cancer cells without harming normal cells. MP1 interacts with lipids that are abnormally distributed on the surface of cancer cells, creating gaping holes that allow molecules crucial for cell function to leak out.
A cancer therapy that could damage the lipid composition of a cell membrane would be a new chapter in finding an anticancer drug. It could be the start in developing new combination therapies, where multiple drugs are used …show more content…
MP1 acts against microbial pathogens by disrupting the bacterial cell membrane. The antimicrobial peptide shows promise for protecting humans from cancer as it can inhibit the growth of prostate and bladder cancer cells, as well as multi-drug resistant leukemic cells. However, it was unclear how MP1 selectively destroys cancer cells without harming normal cells.
Researchers Beales and João Ruggiero Neto from the São Paulo State University in Brazil suspected that the reason might have something to do with the unique properties of cancer cell membranes. In healthy cell membranes, phospholipids called phosphatidylserine (PS) and phosphatidylethanolamine (PE) are located in the inner membrane leaflet facing the inside of the cell. But in cancer cells, PS and PE are embedded in the outer membrane leaflet facing the cell surroundings.
How was the research tested?
The researchers tested their theory by creating model membranes, some of which contained PE and/or PS, and exposing them to MP1. They used a wide range of imaging and biophysical techniques to characterize MP1's destructive effects on the membranes. Strikingly, the presence of PS increased the binding of MP1 to the membrane by a factor of 7 to 8. On the other hand, the presence of PE enhanced MP1's ability to quickly disrupt the membrane, increasing the size of holes by a factor of 20 to