A metabolite of cholesterol promotes breast cancer metastasis through its actions on the endocrine and immune systems

Speaker: 
Dr. Erik Nelson, University of Illinois Cancer Center, Department of Molecular & Integrative Physiology
Location: 
RHPH 164
Date / Time: 
Tuesday, November 21, 2017 - 4:00pm
Host: 
Dr. Mike Wendt
Abstract: 

Obesity and elevated circulating cholesterol are risk factors for breast cancer recurrence, while the use of statins, cholesterol biosynthesis inhibitors widely used for treating hypercholesterolemia, is associated with improved disease-free survival. In this seminar, I will highlight our recent work demonstrating that cholesterol mediates the metastatic effects of a high-fat diet via its oxysterol metabolite, 27-hydroxycholesterol. Intriguingly, the robust effects of 27-hydroxycholesterol on metastasis requires myeloid immune cell function, and we have found that this oxysterol increases the number of polymorphonuclear-neutrophils and γδ-T cells at distal metastatic sites. The pro-metastatic actions of 27-hydroxycholesterol requires both polymorphonuclear-neutrophils and γδ-T cells, and 27-hydroxycholesterol treatment results in a decreased number of cytotoxic CD8+T lymphocytes. Therefore, through its actions on γδ-T cells and polymorphonuclear-neutrophils, 27-hydroxycholesterol functions as a biochemical mediator of the metastatic effects of hypercholesterolemia.

Mega Menu Visual Content