Scientists have long known that something goes awry in normal cells that turn cancerous, but they haven't been able to quite put their fingers on it ... until now.
Mark Muller, a UCF professor in the molecular biology and microbiology program, and his colleagues have found that increased levels of an ancient protein in the nucleus of human cells can stop uncontrollable division of cancerous cells and growth of such tumors.
Their finding could potentially lead to the development of gentler and more effective drugs and therapies for cancer patients. It can also help scientists better understand the science of cancer and aging.
"We have now identified a protein, called MKRN1, that acts on telomerase to promote its degradation," said In Kwong Chung, a professor at Yonsei University in Seoul, South Korea, and a corresponding author of the study, in an e-mail.
Telomerase is an enzyme that protects caps at the end of compact segments of DNA called chromosomes. Normal cells lose this protection early on and die following a certain number of replications.
But that is not the case in cancer cells. These cells, as scientists have long known, keep their armor - telomerase - and as a result can replicate without control. This is where the newly uncovered protein, MKRN1, can come to the rescue.
In their studies, Muller and his colleagues have shown that cancerous cells injected with the MKRN1 gene "were no longer cancer cells, and if given sufficient time in culture, these cells will eventually lose their proliferative capacity," Muller said.
"If we can manipulate the MKRN1 in the body of cancer patients, we might make malignant cells [go away]," Chung wrote in his e-mail.
MKRN1 is an ancient gene and could date back to the beginning of time. The gene is even found in yeast, a simple one-cell organism that is among one of the earlier forms of life.
Conservation of this gene through time means that "change in that gene is not tolerated. It means that it's doing something that's fundamentally important," Muller said.
And a timely death is a necessity for cells because it "enables [our body] to get rid of cells that have already extended their lifespan and might [be subject] to mutation and lead to cancer," explained Muller.
Muller said since the publication of the research in this month's Genes & Development, he has been receiving calls from researchers and cancer patients worldwide.
Although he is excited to share the finding with other researchers, Muller admits that he is at least five years away from developing a drug or treatment. "Much effort in the future will be required to shed light on how MKRN1 may be used as a therapeutic target for checking the uncontrolled division of tumor cells," Chung added.
Regarding the possible applications of the research to anti-aging products, Muller said, "Cellular aging (continuous cell division) can lead to mutations affecting growth control, and this can transform the cells to cancer."
The group is waiting for a multimillion dollar grant from the National Institute of Health to continue its studies.
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