Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1995-9-12
pubmed:abstractText
The mechanism of the antiproliferative activity of tamoxifen on melanoma cells in vitro and in vivo is poorly understood, as it is not mediated by the antiestrogenic properties of tamoxifen. Using a whole-cell assay and nuclear and cytosolic radio-binding experiments with [3H]-estradiol as tracer, we found that MNT1, M10, and M14 melanoma cell lines as well as primary tumors expressed type II estrogen binding sites that bind tamoxifen and the flavonoid quercetin with similar affinity (KD 10-25 nM). Cell count and clonogenic assay showed both compounds to inhibit melanoma cell growth in a concentration-dependent manner in the range of concentrations between 1 nM and 1 microM. Neither the pure antiestrogen ICI-182780 nor the 3-rhamnosylglucoside of quercetin, rutin, bound to type II estrogen binding sites or inhibited cell growth. Our results suggesting that tamoxifen and quercetin can inhibit melanoma cell growth by interacting with type II estrogen binding sites help explain the reported effectiveness of tamoxifen, particularly in estrogen-receptor-negative tumors, and stress the potential role of quercetin in the treatment of melanoma.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0022-202X
pubmed:author
pubmed:issnType
Print
pubmed:volume
105
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
248-53
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1995
pubmed:articleTitle
Tamoxifen and quercetin interact with type II estrogen binding sites and inhibit the growth of human melanoma cells.
pubmed:affiliation
Department of Human Pathology, G. D'Annunzio University, Chieti, Italy.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't