University of Pittsburgh Cancer Institute (UPCI) researchers have uncovered a technique to halt the growth of cancer cells—a discovery that could lead to potential new anti-cancer therapies.
The team discovered when cancerous cells are deprived of Dynamin-related protein 1 (Drp1), they are unable to properly divide and multiply.
How this works comes back to high school biology and the networks of mitochondria each cell contains. Within the cell, mitochondria are essential for energy production. According to the study, Drp1 helps mitochondria undergo fission—a process by which they split themselves into two.
In breast and lung cancer cells deprived of Drp1, the researchers observed a significant network of fused mitochondria. According to the study, this suggests the division of cancer cells stalled. Cells that continue to try and divide end up tearing their chromosomes apart.
“It’s the first time that anybody’s seen a link between mitochondrial fission and cell division,” said UPCI researcher Dr. Bennett Van Houten. “And if you don’t allow your mitochondria to divide, it actually triggers a response in the cell to undergo an arrest.”
Van Houten added the discovery makes mitochondria the new target in the fight against cancer—a target that can be attacked with a potential new drug.
“What we’ve discovered is a compound that actually works like Drp1 and causes the same type of arrest, and in combination with an anti-cancer drug, Cisplatin, is very effective at killing tumor cells,” he said.
So, remove the Drp1 from a cell and the cell should die. But that still leaves a major challenge—how can the protein be removed only from cancer cells without harming healthy cells?
“One of the big problems with cancer chemotherapy,” Van Houten said, “is hitting just the tumor cells and not affecting the other cells in your body. So we’re very excited by this.”
While looking for compounds, the researchers found Mdivi-1. When tested in a laboratory setting, the researchers found the drug only attacks cancerous cells, leaving healthy ones alone.
Van Houten noted however, the research team still doesn’t fully understand how Mdivi-1 works.
We found that this compound, [Mdivi-1], still works even though Drp1 isn’t there,” he said. “And that was a really big surprise because that was the way the compound was discovered as supposedly inhibiting Drp1 from working.”
Van Houten said the next step is conducting safety trials of the drug in animals. This process, he said, would take place over the next two to three years. He added human trials wouldn’t begin for at least five years.
More information about the research done at UPCI can be found in the cover story of the February issue of the Journal of Cell Science.
