Journal
TRENDS IN ENDOCRINOLOGY AND METABOLISM
Volume 25, Issue 12, Pages 649-655Publisher
ELSEVIER SCIENCE LONDON
DOI: 10.1016/j.tem.2014.10.001
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Funding
- Department of Defense Idea Expansion Award [W81XWH-13-1-0366]
- National Cancer Institute of the National Institutes of Health [K99CA172357]
- National Institute of Diabetes and Digestive and Kidney Diseases of the National Institutes of Health [R37DK048807]
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Cholesterol is a risk factor for breast cancer although the mechanisms by which this occurs are not well understood. One hypothesis is that dyslipidemia results in increased cholesterol content in cell membranes, thus impacting upon membrane fluidity and subsequent signaling. In addition, studies demonstrate that the metabolite, 27-hydroxycholesterol (27HC), can function as an estrogen, increasing the proliferation of estrogen receptor (ER)-positive breast cancer cells. This was unexpected because 27HC and other oxysterols activate the liver X receptors (LXR), resulting in a reduction of intracellular cholesterol. Resolution of this paradox will require dissection of the molecular mechanisms by which ER and LXR converge in breast cancer cells. Regardless, the observation that 27HC influences breast cancer provides a rationale for strategies that target cholesterol metabolism.
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