Is there a link between high cholesterol and colon cancer?
A new scientific report warns that people eating a high-cholesterol diet are at an increased risk of developing colon cancer.
The results showed that boosting mice’s cholesterol levels caused intestinal stem cells to divide more quickly, allowing tumors to form much faster.
The study, published in the journal Cell Stem Cell, has identified a molecular pathway that could serve as a new drug target for colon cancer treatment.
“We were excited to find that cholesterol influences the growth of stem cells in the intestines, which in turn accelerates the rate of tumor formation by more than 100-fold,” said Peter Tontonoz, from the University of California.
“While the connection between dietary cholesterol and colon cancer is well established, no one has previously explained the mechanism behind it.”
The scientists increased cholesterol in the intestinal stem cells in some of the mice by introducing more of the substance into their diets.
In others, the researchers altered a gene that regulates phospholipids, the primary type of fat in cell membranes, which spurred the cells into producing more cholesterol on their own.
The stem cells’ ability to multiply increased in both groups.
As the animals’ cholesterol levels rose, their cells divided more rapidly, causing the tissue lining their guts to expand and their intestines to lengthen. These changes significantly sped up the rate of tumor formation in their colons.
University of California - Los Angeles Health Sciences. (2018, January 25). Study could explain link between high-cholesterol diet and colon cancer: Fats spur cells to divide faster, speeding tumor growth. ScienceDaily. Retrieved January 26, 2018 from www.sciencedaily.com/releases/2018/01/180125135551.htm
Bo Wang, Xin Rong, Elisa N.D. Palladino, Jiafang Wang, Alan M. Fogelman, Martín G. Martín, Waddah A. Alrefai, David A. Ford, Peter Tontonoz. Phospholipid Remodeling and Cholesterol Availability Regulate Intestinal Stemness and Tumorigenesis. Cell Stem Cell, 2018; DOI: 10.1016/j.stem.2017.12.017