Source:http://linkedlifedata.com/resource/pubmed/id/19851860
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
3
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pubmed:dateCreated |
2010-7-14
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pubmed:abstractText |
The specific role of dietary fat in breast cancer progression is unclear, although a low-fat diet was associated with decreased recurrence of estrogen receptor alpha negative (ER(-)) breast cancer. ER(-) basal-like MDA-MB-231 and MDA-MB-436 breast cancer cell lines contained a greater number of cytoplasmic lipid droplets compared to luminal ER(+) MCF-7 cells. Therefore, we studied lipid storage functions in these cells. Both triacylglycerol and cholesteryl ester (CE) concentrations were higher in the ER(-) cells, but the ability to synthesize CE distinguished the two types of breast cancer cells. Higher baseline, oleic acid- and LDL-stimulated CE concentrations were found in ER(-) compared to ER(+) cells. The differences corresponded to greater mRNA and protein levels of acyl-CoA:cholesterol acyltransferase 1 (ACAT1), higher ACAT activity, higher caveolin-1 protein levels, greater LDL uptake, and lower de novo cholesterol synthesis in ER(-) cells. Human LDL stimulated proliferation of ER(-) MDA-MB-231 cells, but had little effect on proliferation of ER(+) MCF-7 cells. The functional significance of these findings was demonstrated by the observation that the ACAT inhibitor CP-113,818 reduced proliferation of breast cancer cells, and specifically reduced LDL-induced proliferation of ER(-) cells. Taken together, our studies show that a greater ability to take up, store and utilize exogenous cholesterol confers a proliferative advantage to basal-like ER(-) breast cancer cells. Differences in lipid uptake and storage capability may at least partially explain the differential effect of a low-fat diet on human breast cancer recurrence.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/ACAT1 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Acetyl-CoA C-Acetyltransferase,
http://linkedlifedata.com/resource/pubmed/chemical/Cholesterol, LDL,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Estrogen
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pubmed:status |
MEDLINE
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pubmed:month |
Aug
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pubmed:issn |
1573-7217
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pubmed:author | |
pubmed:issnType |
Electronic
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pubmed:volume |
122
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
661-70
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pubmed:dateRevised |
2011-7-1
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pubmed:meshHeading |
pubmed-meshheading:19851860-Acetyl-CoA C-Acetyltransferase,
pubmed-meshheading:19851860-Blotting, Western,
pubmed-meshheading:19851860-Breast Neoplasms,
pubmed-meshheading:19851860-Cell Proliferation,
pubmed-meshheading:19851860-Cholesterol, LDL,
pubmed-meshheading:19851860-Female,
pubmed-meshheading:19851860-Humans,
pubmed-meshheading:19851860-Neoplasms, Basal Cell,
pubmed-meshheading:19851860-RNA, Messenger,
pubmed-meshheading:19851860-Receptors, Estrogen,
pubmed-meshheading:19851860-Reverse Transcriptase Polymerase Chain Reaction,
pubmed-meshheading:19851860-Tumor Cells, Cultured
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pubmed:year |
2010
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pubmed:articleTitle |
High ACAT1 expression in estrogen receptor negative basal-like breast cancer cells is associated with LDL-induced proliferation.
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pubmed:affiliation |
Cellular Biochemistry Laboratory, Methodist Research Institute, 1800 N. Capitol Ave, E504, Indianapolis, IN 46202, USA. cantalis@clarian.org
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pubmed:publicationType |
Journal Article,
Comparative Study,
Research Support, Non-U.S. Gov't
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