A Common Cholesterol Drug May Weaken Ovarian Cancer Spread

The drug, bezafibrate, could help dismantle a hidden protective shield around the cancer cells

Two scientists working in a lab
Yasaman Setayeshpour, left, and Jen-Tsan Chi led the study.

The following is a summary of a story written by Shantell Kirkendoll on Duke University School of Medicine.

Women with advanced ovarian cancer experience an uncomfortable buildup of fluid in the abdomen, called ascites. Duke researchers found that this fluid also helps cancer cells survive and spread but a common cholesterol drug could help disrupt the process.   

Researchers at Duke Cancer Institute found that a drug called bezafibrate may weaken the environment tumors rely on, potentially making them more responsive to existing treatments.

The study shows that ascites form a protective shield around free-floating ovarian cancer cells. These metastatic cells are typically vulnerable to ferroptosis, a form of cell death usually accompanied by iron accumulation and damage to fats (lipids) in cell membranes.

But when immersed in ascites, cancer cells evade this fate. Even small amounts of the fluid, far less than those found in patients, can block ferroptosis by altering how cells process fats and regulate iron. 

By isolating the components of ascites, researchers discovered that lipids are the primary drivers of this protective effect. When lipids were removed, cancer cells once again became susceptible to ferroptosis. This insight led the team to test whether targeting lipid metabolism could dismantle the cancer’s defenses. 

“We’ve learned it gives cancer a survival advantage, which fills a major gap in understanding how ovarian cancer spreads,” said senior study author Jen-Tsan Chi, a professor in the Department of Molecular Genetics and Microbiologyand co-leader of the Cancer Biology Program at the Duke Cancer Institute.

While bezafibrate, a decades-old drug commonly used to lower triglycerides, had little effect on its own, it restored cancer cells’ sensitivity to the cell death. 

Although the findings are based on laboratory models and do not yet demonstrate a direct clinical treatment, they point to a promising new strategy: targeting the tumor microenvironment. To learn more about this research, visit Duke University School of Medicine.