Apoptosis is a unique process within the body’s cell system that is essentially a form of “cell suicide”. Cells do not like to live alone. In the early stages of the formation of a tumor a cell may be pushed out of its “home” because it grows too large. The cell normally responds to this displacement by destroying its own nucleus and DNA and it is then absorbed, eaten if you will by immune cells. This usually stops cancer cells in their tracks, before they have a chance to proliferate.

New research from Harvard University has now uncovered another way that these homeless precancerous  cells are “killed”. By studying the two different types of human breast epithelial cells they found that when they are taken away from their “home” environment the cells actually lose the ability to harvest energy from their surroundings, essentially starving.

“We originally thought that in order for cells to survive outside their normal environment, they would simply need to suppress apoptosis,” says Joan Brugge, senior author on the paper, which appeared August 19 online in the publication Nature. “But our studies indicate that this activity is not sufficient to prevent the demise of homeless cells. Even if they escape apoptosis, these cells can’t transport enough glucose to sustain an energy supply.”

She and her team were also surprised to find that metabolic function of these cells can be restored if antioxidant levels are increased inside them, as this allows the cells to draw from energy pathways that do not rely on glucose.

Says Zachary Schafer for was a post doc in Professor Bruge’s lab at the time of the study but is now an assistant professor at the University of Notre Dame “It raises the interesting idea that antioxidants, which are typically thought to be protective because they prevent genomic damage, might be allowing these potentially dangerous cells to survive,”

The authors are quick to caution that their research was not designed to mimic dietary anti oxidants in the body. They used two specific antioxidant compounds that are chemically very different from those in food and dietary supplements.

“We think that genes with antioxidant activity play a much bigger role than antioxidant compounds administered from outside the body,” says Brugge. “What happens with dietary antioxidants is much more complicated and not what we were trying to study.”

The next step for Bruge is take these preliminary studies further, in the hope that by better understanding the structures of cancer cells new drugs can be developed to target them.