Two genes that appear to help intestinal stem cells burn dietary fat may play a role in colon cancer, according to new research.
The study in the journal Gastroenterology describes a new connection between the way in which cells consume fat and how genes regulate stem cell behavior in the intestines of mice.
“This is important because scientists have shown that when there’s too much dietary fat in the intestine, stem cell numbers increase, boosting susceptibility to colon cancer,” says senior author Michael Verzi, an associate professor in the genetics department at Rutgers University-New Brunswick.
People naturally lose millions of intestinal cells daily, much like they lose skin cells. Intestinal stem cells undergo constant renewal and fuel the continuous turnover of the lining of the intestine, but altered stem cell functions can lead to colon cancer.
Colorectal cancer (of the colon or rectum) is the third most common cancer diagnosed in both men and women in the United States. An estimated 101,420 Americans will get a colon cancer diagnosis this year, according to the American Cancer Society.
Recent studies have shown that intestinal stem cells can increase in animals on a high fat “Western” diet. This could potentially explain an elevated cancer risk from such a diet.
The researchers recently discovered that two genes (HNF4A and HNF4G) work together to promote the proper function of the intestinal lining. In the new study, they found that mice lost intestinal stem cells when these genes were inactivated, confirming their importance. The scientists believe that the genes help stem cells burn fat, providing them energy.
Going forward, the researchers hope to further investigate whether the two genes alter stem cell numbers and cancer risk during a high fat diet, says Verzi, a research member in the Genomic Instability and Cancer Genetics Research Program at Rutgers Cancer Institute of New Jersey and a member of the Rutgers Center for Lipid Research.
Source: Rutgers University
