A research team's discovery of a protein's role in controlling whether or not cells multiply could lead to a new understanding of how to combat cancer.
Dr. Aaron Putzke, assistant professor of biology at Hope College, and Dr. Joel H. Rothman, professor of biology and chair of the Department of Molecular, Cellular and Development Biology at the University of California-Santa Barbara, have gained new insights into the way that a protein called Fer affects how cells behave. The findings are reported in an article being published in the "Proceedings of the National Academy of Sciences."
According to Putzke, the Fer protein was previously known to help keep cells together in the way necessary for normal functioning. He and Rothman, however, have discovered that Fer also helps prevent cells from reproducing excessively. With rampant cell growth a characteristic of cancer, the researchers hope that they have uncovered a clue as to how the disease might one day be controlled.
"Excessive cell division is such a hallmark of cancer that we immediately got excited," Putzke said of the discovery.
Putzke and Rothman uncovered the connection through their studies of a microscopic roundworm called Caenorhabditis elegans. Putzke noted that the species is a good subject for multiple reasons: it's common and thus readily available; it's transparent and therefore easily viewed through a microscope; it matures in 3 days, making it easy to study its cellular behavior; and its development is consistent - every adult worm has about 1,000 cells.
Or at least, every worm is supposed to. It's the latter quality that led the researchers to view Fer in a new way.
"I was looking at different tissue types in a sample of mutant embryos and I noticed too many gut cells in each," Putzke said.
"An advantage in every worm having the same number of cells is that you can work backwards and figure out what went wrong," he said. "Our research showed a different role for this protein."
Fer, Putzke noted, is important in controlling a cell-signaling mechanism called Wnt. When Fer is absent, he and Rothman found, Wnt hyper-activates and tells the cells to divide and make too many new cells.
Putzke noted that other studies have shown altered levels of Fer in a variety of cancers. With Fer understood to help hold cells together, he said, scientists reasoned that Fer's role in the disease related to the protein's reduced ability to assure cells' cohesion. Given the new findings, he said, it's possible that the problem is instead that a reduced amount of Fer allows cancer cells to multiply.
The next step, Putzke noted, is to figure out how to use the information.
"What we could do next is look at how the protein is functioning specifically," he said. "We've identified the cellular pathway that is affected, and the next question is, how could you target that in a situation to prevent it, which is important in both developing organisms and cancer?"