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Study says normal but out-of-control enzyme may be culprit that signals some cells to become cancer

Working with human colorectal cancer cells, a University of Minnesota team, led by cancer biologists Zigang Dong and Ann Bode, has found the potential culprit among a network of enzymes that relay signals inside cells to regulate such functions as cell growth, cancer development and programmed cell death. The work suggests that drugs designed to disable the enzyme, known as TOPK, could have anti-cancer benefits. The study appears in the July issue of the journal Gastroenterology.

Colorectal [cancer] is the second leading cause of cancer mortality, and the molecular pathways [by which it develops] remain incompletely understood, said Dong, a McKnight Presidential Professor in cancer prevention and director of the universitys Hormel Institute in Austin, Minn. In this study, we provided evidence showing that TOPK promotes transformation [of normal cells to cancerous ones] in colorectal carcinoma.

The story begins with the frequent observation by researchers that members of this enzyme network are overactive in the cells of several human cancers. The function of all these enzymes is to activate other enzymes and proteins, which makes them ideal for passing along signals.

For example, a cancer-causing agent or a hormone may find its way from the bloodstream to the outer membrane of a cell. After its arrival, it sets off a chain of reactions, or signals, inside the cell. Some of these signals take the form of certain enzymes activating others. Eventually, the news reaches the genetic material inside the cell nucleus, where changes resulting in uncontrolled growth--cancer--or some other cell behavior are made.

It was thought that some form of an enzyme called MEK, which belongs to the family of signaling enzymes, was the culprit. But to cause cancer, an enzyme or other agent is expected to be active all the time, like a light with no off switch. MEK, however, is never active all the time in nature; only if kept artificially activ
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Contact: David Ruth
druth@umn.edu
612-624-1690
University of Minnesota
31-Jul-2007


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