The study was conducted by a team of researchers led by Zigang Dong and Ann Bode at the University of Minnesota.
TOPK is not very active in normal tissues, but it is quite active in cancerous cells taken from blood, breast, prostate and colorectal tumours, among others. The onset of cancer could trigger the permanent turning-on of this enzyme.
It was earlier thought that an enzyme called MEK, which belongs to the family of signalling enzymes, triggered cancer. But to cause cancer, an enzyme is expected to be active all the time. MEK, however, is never active all the time in nature; only if kept artificially active can it lead to the disease.
As part of the study researchers examined the role of TOPK to determine whether its high activity could lead to cancer.
Researchers engineered mouse skin cells to produce excessive amounts of the enzyme and then injected the cells into other mice, which developed tumours.
They then 'silenced' the gene for TOPK in human colorectal cancer cells, and found that growth of the cells was significantly slowed compared to control colorectal cancer cells.
The study also found that TOPK and a related enzyme (not MEK) activated each other in growing human colorectal cancer cells.
"In this study, we provided evidence showing that TOPK promotes transformation [of normal cells to cancerous ones] in colorectal carcinoma," Dong said.
The findings of the study were published in the July issue of the journal Gastroenterology.