Linked Life Data

1312718

Source:http://linkedlifedata.com/resource/pubmed/id/1312718

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
1992-4-17
pubmed:abstractText
The binding of luteinizing hormone-releasing hormone (LH-RH) analogues to the human mammary tumor cell line MCF-7 and their effect on the cell proliferation was studied to elucidate their direct action on estrogen-dependent mammary tumors. The growth rate of these cells was doubled by the addition of 1 nM estradiol to cells maintained in an estrogen-deficient medium. Although the basal growth rate was only slightly inhibited by the LH-RH antagonist [Ac-D-Nal(2)1,D-Phe(pCl)2,D-Pal(3)3,D-Cit6,D-Ala10]LH-RH (SB-75), the estrogen-stimulated growth was completely abolished by the antagonist. In contrast, the LH-RH agonist buserelin stimulated cell growth in estrogen-deficient medium, whereas it had no effect in the presence of estrogen. 125I-labeled buserelin was used for the measurement of LH-RH receptors on MCF-7 cells. A Scatchard plot analysis of buserelin-specific binding revealed a nonlinear plot, which suggested the presence of one high-affinity binding site with a Kd of 1.4 +/- 1.0 nM and the remaining sites with low affinity (Kd = 1.3 +/- 1.0 microM). The binding of 125I-labeled buserelin was displaced equally well by unlabeled buserelin and by the LH-RH antagonist SB-75, suggesting that both analogues are bound to the same receptor. When parallel experiments were performed with 125I-labeled SB-75, the binding was displaced by unlabeled SB-75 and other antagonists, but only partially displaced by unlabeled buserelin. The results suggest that in these mammary tumor cells there is a LH-RH antagonist binding site that is not recognizable by LH-RH agonists. This hypothesis was tested by measuring cell growth in the presence of both agonists and antagonists. It was found that SB-75 inhibited the stimulation of growth by buserelin, but buserelin did not prevent the inhibition by the antagonist of the estrogen-dependent growth. These results suggest that antagonists directly inhibit mammary tumor growth, not only by competing with LH-RH high-affinity receptors, but also by other mechanisms mediated by low-affinity antagonist binding sites.
pubmed:commentsCorrections
http://linkedlifedata.com/resource/pubmed/commentcorrection/1312718-2194783, http://linkedlifedata.com/resource/pubmed/commentcorrection/1312718-2569034, http://linkedlifedata.com/resource/pubmed/commentcorrection/1312718-2646641, http://linkedlifedata.com/resource/pubmed/commentcorrection/1312718-2982100, http://linkedlifedata.com/resource/pubmed/commentcorrection/1312718-3029154, http://linkedlifedata.com/resource/pubmed/commentcorrection/1312718-3082618, http://linkedlifedata.com/resource/pubmed/commentcorrection/1312718-3119199, http://linkedlifedata.com/resource/pubmed/commentcorrection/1312718-3278323, http://linkedlifedata.com/resource/pubmed/commentcorrection/1312718-3304294, http://linkedlifedata.com/resource/pubmed/commentcorrection/1312718-3549276, http://linkedlifedata.com/resource/pubmed/commentcorrection/1312718-3802100, http://linkedlifedata.com/resource/pubmed/commentcorrection/1312718-6254391, http://linkedlifedata.com/resource/pubmed/commentcorrection/1312718-6269924, http://linkedlifedata.com/resource/pubmed/commentcorrection/1312718-6443575, http://linkedlifedata.com/resource/pubmed/commentcorrection/1312718-6461861
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0027-8424
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
89
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2336-9
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed:year
1992
pubmed:articleTitle
Direct effects of luteinizing hormone-releasing hormone agonists and antagonists on MCF-7 mammary cancer cells.
pubmed:affiliation
Clinical Biochemistry Department, Faculty of Health Sciences, Soroka Medical Center, Ben-Gurion University of the Negev, Beer-Sheva, Israel.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't