Researchers find that cancer cells from patients with pancreatic tumors grow when they have an oxygen deficiency. When these cells lack oxygen and nutrients, they must change their energy supply so they can continue to grow.
Mitochondria burn oxygen and provide energy for the body. Scientists from the Max Planck Institute for Biology of Ageing have discovered that mitochondria are reprogrammed when it’s lacking oxygen and nutrients. Pancreatic tumors may use this same technique to keep growing with little oxygen and nutrients reaching the cells.
Cells react to oxygen deficiency by changing their energy supply to glycolysis. Glycolysis is when sugar is fermented without oxygen. This happens when the cells in the body are supplied with less oxygen and nutrients. The same thing can happen with cancer cells because tumors have poor blood supply and less oxygen and nutrients reach the cells.
“It has been known for some time that cells reduce the number of mitochondria when they lack oxygen and switch to glycolysis,” says Max Planck Director Thomas Langer. “We have now discovered that the remaining mitochondria are additionally reprogrammed to meet the new requirements.”
Researchers have discovered a new signaling pathway where a protease in the membrane of mitochondria is activated during the conversion to glycolysis and then breaks down various proteins in the organelles. Because of this no new mitochondria are formed, and the remaining mitochondria must change their metabolism.
“This signaling pathway not only has a built-in timer, but also enables a very rapid response to oxygen deficiency,” said Langer.
By switching off the signaling pathway to the mitochondria, scientists were able to slow the growth of pancreatic tumor cells. Researchers believe that the newly discovered signaling pathway could lead to therapies against pancreatic cancer.
“There is currently no treatment available for pancreatic cancer. I believe that this protease can be a very interesting therapeutic target because we have seen that the signaling pathway is also active in human patients with pancreatic cancer,” says Langer. “However, there are no known substances that have an effect on this protease.”
Story Source: ScienceDaily
Photo: Biology of Ageing/Thomas MacVicar
