Two enzymes that trigger cancer found
Scientists from Huntsman Cancer Institute at the University of Utah have discovered two enzymes which, when combined, play a role in early stages of cancer. This discovery could lead to better understanding of cancer genesis, thus providing more knowledge for drug (cure) creation.
“We could conceivably reactivate a completely normal gene in a tumor cell – a gene that could prevent the growth of a tumor if reactivated,” said David Jones, Ph.D., professor of oncological sciences. “We believe this could be one of the earliest processes to go wrong in cancer,” he adds. By manipulating these enzymes, we could possibly prevent or slow the onset of tumors.”
The two enzymes seem to have a switch under their control — a switch that turns critical genes on or off.
Zebrafish (share similar characteristics to humans) was used by the HCI scientists to identify a previously unknown enzyme process that controls the levels of DNA methylation on genes.
“Methylation is a cellular process that is required for healthy cell growth and development, but it can go awry in cancer and diseased cells,” says Brad Cairns, Ph.D., HCI investigator and professor of oncological sciences at the University of Utah. “You can think of DNA methylation as an on-and-off switch. Methylation silences or ‘shuts off’ genes that need to be turned off or are not functioning as they should, whereas the reverse process called demethylation ‘turns on’ healthy genes and genes needed at critical times in development,” he says.
In cancer, this methylation process goes “wild”, leading to tumor growth. Genes that should be “turned on” are not and vice versa.
In the future, scientists will focus on discovering whether the DNA methylation levels can be manipulated genetically or not. If yes, it could lead to drugs to reactivate particular genes and suppress tumor growth. Remarkably, this system also helps protect the genome from mutations.
“We discovered a pair of enzymes that can remove methylated DNA, but if these enzymes work improperly, they will instead enhance the rate of mutations in methylated DNA and cause cancer progression,” says Jones. “The question now is, when they work improperly, can we find ways to shut them off and prevent these mutations?”
The project is published in this month’s issue of Cell.
Source: unews.utah.edu
