Switch to
Predicate | Object |
---|---|
rdf:type | |
lifeskim:mentions | |
pubmed:issue |
20
|
pubmed:dateCreated |
1997-11-10
|
pubmed:abstractText |
To understand the signaling and growth-inhibitory effects of retinoids, we have examined the metabolism of [3H]retinol in a number of estrogen receptor-positive (ER+) and estrogen receptor-negative (ER-) human breast cancer cell lines. We have also assayed the metabolism of [3H]retinol in normal human mammary epithelial cells. The ER+ breast cancer cell lines MCF-7 and T47D produce [3H]4-oxoretinol from [3H]retinol; the production of [3H]4-oxoretinol is increased by initial culture in the presence of nonradiolabeled retinoic acid (RA) or N-(4-hydroxyphenyl)retinamide, indicating that these drugs enhance [3H]retinol metabolism to [3H]4-oxoretinol. No metabolism of [3H]retinol to [3H]RA in these ER+ tumor lines was detected. ER- breast cancer lines MDA-MB-231, MDA-MB-468, and BT20 do not metabolize [3H]retinol to [3H]4-oxoretinol. In the ER- tumor lines, most of the [3H]retinol remains unmetabolized during the 24-h culture period; MDA-MB-468 and BT20 metabolize some [3H]retinol to [3H]RA. Unlike the majority of the tumor lines, the normal human breast epithelial cell strains AD074 and MCF10A rapidly metabolize [3H]retinol to [3H]retinyl esters. No detectable [3H]RA is produced from [3H]retinol in AD074 and MCF10A cells. Thus, the normal breast epithelial strains, the ER+ tumor lines and the ER- tumor lines differ greatly in their pathways of [3H]retinol metabolism. The levels of cellular retinol binding protein-I mRNA expression are not correlated with the levels or types of various retinol metabolites. Whereas the normal breast epithelial cells and the ER+ tumor lines are growth inhibited by RA, N-(4-hydroxyphenyl)retinamide, and 4-oxoretinol, only the 4-oxoretinol is growth inhibitory in the ER- tumor lines. The cellular retinoic acid-binding protein II mRNA levels are not correlated with the growth inhibition by RA or 4-oxoretinol in the normal and tumor lines.
|
pubmed:grant | |
pubmed:language |
eng
|
pubmed:journal | |
pubmed:citationSubset |
IM
|
pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/4-oxoretinol,
http://linkedlifedata.com/resource/pubmed/chemical/RBP1 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/RBP2 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/Retinol-Binding Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Retinol-Binding Proteins, Cellular,
http://linkedlifedata.com/resource/pubmed/chemical/Tritium,
http://linkedlifedata.com/resource/pubmed/chemical/Vitamin A
|
pubmed:status |
MEDLINE
|
pubmed:month |
Oct
|
pubmed:issn |
0008-5472
|
pubmed:author | |
pubmed:issnType |
Print
|
pubmed:day |
15
|
pubmed:volume |
57
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
4642-51
|
pubmed:dateRevised |
2007-11-15
|
pubmed:meshHeading |
pubmed-meshheading:9377581-Breast,
pubmed-meshheading:9377581-Breast Neoplasms,
pubmed-meshheading:9377581-Cell Division,
pubmed-meshheading:9377581-Cell Line,
pubmed-meshheading:9377581-Chromatography, High Pressure Liquid,
pubmed-meshheading:9377581-Epithelial Cells,
pubmed-meshheading:9377581-Female,
pubmed-meshheading:9377581-Humans,
pubmed-meshheading:9377581-Kinetics,
pubmed-meshheading:9377581-RNA, Messenger,
pubmed-meshheading:9377581-Retinol-Binding Proteins,
pubmed-meshheading:9377581-Retinol-Binding Proteins, Cellular,
pubmed-meshheading:9377581-Transcription, Genetic,
pubmed-meshheading:9377581-Tritium,
pubmed-meshheading:9377581-Tumor Cells, Cultured,
pubmed-meshheading:9377581-Vitamin A
|
pubmed:year |
1997
|
pubmed:articleTitle |
Human breast cancer cells and normal mammary epithelial cells: retinol metabolism and growth inhibition by the retinol metabolite 4-oxoretinol.
|
pubmed:affiliation |
Department of Pharmacology, Cornell University Medical College, New York, New York 10021, USA.
|
pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.
|