Mar 212012
 
Authors: Colleen Canty

In an inconspicuous room, cramped with a monstrous microscope and ratty rolling chair, wedged into a narrow corridor of a building on the outskirts of campus, one team of CSU scientists is closing in on a cure for cancer and Alzheimer’s disease.

Well, they’re getting closer, at least.

Last week, the team of four researchers and professors recently published new findings appearing in Developmental CELL Journal on cofilin, a protein that, when mutated in a cell, can lead to developmental defects and diseases such as Alzheimer’s, cancer and spina bipheta.

The protein is in charge of breaking down the cell polymer F-actin, a type of “scaffolding” that dictates the shape of a cell.

“It (F-actin) is like the poles in a tent – they provide framework and the shape of the tent is dictated by this scaffolding,” explained O’Neil Wiggan, the research scientist on the team who conducted many of the experiments and headed up the writing of the research. “We’ve observed in various diseases that cofilin’s activity becomes deregulated.”

Scientists in the research field have widely accepted cofilin’s identity as merely an agent of this disassembly within a cell since the protein’s discovery in the 1980s.

But now, the CSU team is illuminating its other essential role that’s been overlooked for the past 30 years.

During one particular experiment, in what Wiggan describes as “quite an enlightening moment,” the team witnessed cofilin’s influential role in cell division –– when the protein was deregulated, chromosomes in the daughter cells became imbalanced during cell division.

“What’s so exciting about our new research is it shows the disassembly of the F-actin structure is no longer the only thing that cofilin dictates,” Wiggan said. “We now know it also regulates the myosins –– the molecular motors –– that allow a cell to migrate around the body.”

To put it simply, this research proves there is more to the protein than anyone thought. Such a discovery calls for a complete reevaluation of its role in diseases –– and exactly which defects treatments should be targeting to cure them.

“The entire field has to go back now and think about how the protein works in specific defects –– we have to start asking whether it is a problem with disassembly or regulation of motors,” Wiggan said. “In theory, we can start regulating cofilin to develop effective therapeutics and treatments for diseases.”

This doesn’t mean the team has found the cure to cancer, necessarily. But what it does mean is they’ve found validation in their past two years of research on cofilin.

They’re moving in the right direction.

According to Jim Bamburg, a biochemistry professor and one of the first scientists to identify the protein in the 80s, this research is a new way of looking at cofilin that previous observations have overlooked.

“People –– us included –– have been misinterpreting previous observations, and in light of this info, we need to start reevaluating cofilin in general,” Bamburg said.

This breakthrough is no final destination for cofilin research, however. The team, comprised of Wiggan, Bamburg, biochemistry professor Jennifer DeLuca and research associate Alisa Shaw, will continue to work together on what may be a long journey, but one making “substantial progress.”

“I don’t think it will even be another 20 years –– maybe 15 –– until we are in a better position to utilize this knowledge to develop effective therapeutics,” Wiggan said. “We’ve highlighted the importance of basic research and understanding at the molecular level. We’ve proved there is no magic bullet, but we are getting closer and closer.”

Collegian writer Colleen Canty can be reached at news@collegian.com.

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