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Trends Endocrinol Metab. 2014 Dec;25(12):649-55. doi: 10.1016/j.tem.2014.10.001. Epub 2014 Nov 4.

Cholesterol and breast cancer pathophysiology.

Author information

1
Department of Molecular and Integrative Physiology, University of Illinois at Urbana-Champaign, IL 61801, USA.
2
Department of Pharmacology and Cancer Biology, Duke University School of Medicine, Durham, NC 27710, USA.
3
Department of Pharmacology and Cancer Biology, Duke University School of Medicine, Durham, NC 27710, USA. Electronic address: donald.mcdonnell@duke.edu.

Abstract

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.

PMID:
25458418
PMCID:
PMC4268141
DOI:
10.1016/j.tem.2014.10.001
[Indexed for MEDLINE]
Free PMC Article

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