By Anna Kolchinski
For a long time, researchers have been puzzled by the fact that high cholesterol has been known to increase the spread of breast cancer, also known as metastasis. This has widespread consequences, as breast cancer and cancers in general become much more difficult to treat effectively once they spread beyond the region of the primary tumor. New research just published in Nature Communications aimed to find out exactly why high cholesterol levels lower the immune system's ability to fight metastasis. The researchers focused on a byproduct of cholesterol metabolism known as 27HC, which they suspected to be the culprit. First, they fed rats with breast cancer a diet high in cholesterol, confirming by checking against a control group that metastasis rates were in fact higher in the high cholesterol group. They then treated the high-cholesterol rats in two different ways: one with a drug class called statins, which lower cholesterol in general, and one with an enzyme inhibiting the production of 27HC. They found that while both groups showed improvement, the treatment targeted towards 27HC inhibition was more effective in preventing metastasis. They hypothesized that this could be because 27HC tricks the immune system into accepting the cancer and ceasing any attack on growing cancer cells. The researchers found that immune cells were especially damaged in metastatic regions high in 27HC, supporting their hypothesis. If the 27HC pathway acts the same way in humans as it does in mice, the implications would be enormous. Rates of metastasis in breast cancer, as well as other types of cancers, could be dramatically lowered in a non-invasive way.
University of Illinois at Urbana-Champaign. (2017, October 12). Cholesterol byproduct hijacks immune cells, lets breast cancer spread. ScienceDaily. Retrieved October 21, 2017 from www.sciencedaily.com/releases/2017/10/171012125244.htm