A Group of Mice Study Show How Cholesterol May Actually Stop The Spread of Cancer

Ira and Arouk

Scientists examined Petri dishes and mice. They wanted to see the link between high cholesterol levels and cancer cell growth and spread. The analysis was shocking and unexpected because from what they’ve observed, high cholesterol levels fuel cancer cells by increasing resistance to a form of cell death. This means that lowering cholesterol levels is not only beneficial for good health but may also become beneficial in terms of the therapeutic regimen for cancer treatment.


Cholesterol and Cancer

Cholesterol  is a fat-like, waxy substance that is produced in the liver. This assists in the production of hormones and essential vitamins that the body needs. When there are large quantities of cholesterol present in the body, this buildup forms deposits known as plaques, which in turn, block blood vessels. When left untreated, the person can suffer from a heart attack, a stroke, or another related health issue.

There are several studies that implicates high cholesterol levels in some cancers. However, while this may be connected, scientists have yet to fully understand the exact mechanism behind it.

So, scientists from the Duke University School of Medicine in Durham, NC, have decided to research on the matter further and have recently proposed an explanation for this. What they did was study cholesterol regulation in cancer cells and mice. They hypothesized how high cholesterol levels may fuel cancer resistance to cell death, which can worsen disease outcomes. Their recent findings show a previously undiscovered mechanism in which elevated cholesterol levels influence cancer cells in the body.

Lead scientist Dr. Donald McDonnell, Ph.D., a professor of pharmacology and cancer biology talked to Medical News Today and explained the importance of their discovery. He said, “We believe [our work] addresses long standing questions regarding the impact of overnutrition, obesity, and dyslipidemia/hypercholesterolemia on cancer pathobiology.”

The doctor further stated, “There is an abundance of epidemiological evidence linking hypercholesterolemia to poorer outcomes in [people] with most cancers, [and now] we think we have found why and have defined a completely new way to treat these cancers.”

Dr. Lynne Elmore, Ph.D., a senior scientific director of cell biology and preclinical cancer research at the American Cancer Society, also came up with the same conclusion. She explained, “Published data have demonstrated that high cholesterol promotes the growth of estrogen-positive breast and gynecological cancers owing to derivatives of cholesterol that act like estrogen, fueling cancer growth.” She further added, “But in this study, the research team observed that cancers that don’t rely on estrogen for growth (estrogen-negative) are still associated with a worse disease by high cholesterol. This strongly suggests that there is at least one other mechanism of cancer action for high cholesterol, which formed the basis for this comprehensive study.”

The results of the study are elaborated further in the journal Nature Communications.


High Cholesterol Levels and Immunity from Cell Death

In order to fully understand the connection, the researchers carried out their studies. They made use of cell lines and mice models. The results were this: 27HC, a derivative of cholesterol that is obtained through oxidation, is insinuated when it comes to the many forms of cancer.

When they researchers made use of animal models, they observed how constant and long-standing exposure to 27HC resulted in the growth of tumors that were highly metastatic. This means that the cancer cells spread from where they initially formed to the other parts of the body. Interestingly, however, the scientists also discovered that 27HC prompted metabolic stress in cancer cells. Which meant that they were allowed to escape a natural cell death process called ferroptosis. Because of this, the incident increased the tumor-forming ability and metastatic capacity of the cancer cells.

The findings in the study indicated and explained role of cholesterol in cancer cell resistance to cell death, thereby fueling the dangerous cell’s growth and spread. Dr. Elmore also shared with MNT the importance of understanding what makes these cancer cells grow, spread, and metastasize. She said, “If we know the key mediators [of cancer], that could pave the way for developing targeted therapies to treat and perhaps prevent cancers.”


The Study’s Promising Results

The results from the initial experiments made are highly encouraging. But like any new research, the clinical implications of this study have yet to be fully confirmed by more research. For one thing, Dr. McDonnell and the team admit to the fact that they have yet to figure out how resistance to ferroptosis increases the tumor-forming ability and metastatic capacity of the said cancer cells.

Hence, the team plans to further extend their research to other types of cancers that are found outside the breast and gynecological areas.

Still, there is something that is clear even at this point of the study: The results are able to supplement to the existing information available on cholesterol and cancer. More importantly, the findings go a step further when it comes to investigation of the other mechanisms of action of cholesterol in cancer. One day, this may be significant and important enough to find a cure that cancer patients can truly benefit from.