Cancer cells are quite similar to normal cells in many ways, but it’s the small differences that really matter. One of these slight differences is in their metabolism.
Normally, cells use aerobic respiration, aka oxygen-based energy production, to metabolize sugar into energy. This method produces a large amount of energy but requires an abundance of oxygen and other nutrients. Cancer cells use something called glycolysis, which is far less efficient but requires fewer nutrients and no oxygen. This shift from one energy production to another is called the Warburg Effect, and it allows cancer cells to grow quickly with low upkeep.
A team from the University Children’s Hospital in Heidelberg, Germany, thought this metabolic shift could be a good target for new cancer drugs. They hypothesized that the protein ADP-dependent glucokinase (ADPGK), a sort of nutrient sensor involved with controlling the Warburg effect, might be a critical junction for cancer malignancy.
This new study would watch markers of metabolism shift of the Burkitt Lymphoma cells after activation with a synthetic signal. Activation would induce rapid growth in the cancer cells. The team would knock out the ADPGK gene (essentially delete it from the genome), and in theory, the cells would not experience the same explosive growth. This would confirm that ADPGK plays a critical roll in the metabolism of cancer cells.
The study found that ADPGK knockouts inhibited the activation of the Burkitt’s Lymphoma cells in the lab. There was a decrease in cellular growth markers and an increase in apoptosis markers (a programmed cell death pathway). Further analysis led the team to believe this suppression was due to the cancer cells being unable to obtain glucose, an essential fuel in glycolysis and aerobic metabolisms.
The discovery of the critical junction in Burkitt’s Lymphoma metabolism is quite a find. It offers a new source of drug targets for therapy studies and provides us with a better understanding of cancer metabolism in the body.
The study ends, “…we have thus uncovered a novel target in the form of ADPGK on the cross-roads of these pathways, and its targeting via development of novel therapeutics could prove to be indispensable for curbing aggressively growing malignancies.”