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Antiestrogen interaction with estrogen receptors and additional antiestrogen binding sites in human breast cancer MCF-7 cells

Title
Antiestrogen interaction with estrogen receptors and additional antiestrogen binding sites in human breast cancer MCF-7 cells
Authors
Ahn M.R.Sheen Y.Y.
Ewha Authors
신윤용
SCOPUS Author ID
신윤용scopus
Issue Date
1997
Journal Title
Archives of Pharmacal Research
ISSN
0253-6269JCR Link
Citation
Archives of Pharmacal Research vol. 20, no. 6, pp. 579 - 585
Indexed
SCIE; SCOPUS; KCI scopus
Document Type
Article
Abstract
To gain further insight into the mechanism of action of antiestrogens, we examined the interaction of antiestrogen with the estrogen receptor system and with estrogen- noncompetable antiestrogen binding sites. In addition to binding directly to the estrogen receptor, antiestrogens can be found associated with binding sites that are distinct from the estrogen receptor. In contrast to the restriction of estrogen receptors to estrogen target cells, such as those of uterus and mammary glands, antiestrogen binding sites are present in equal amounts in estrogen receptor-positive and -negative human breast cancer cell lines, such as MCF-7, T47D, and MDA-MB-231 that differ markedly in their sensitivity to antiestrogens. In order to gain greater insight into the role of these antiestrogen binding sites in the action of antiestrogens, we have examined the biopotency of different antiestrogens for the antiestrogen binding sites and that is C1628 > tamoxifen > trans-hydroxy tamoxifen > C1628M > H1285 > LY117018. This order of affinities does not parallel the affinity of these compounds for the estrogen receptor nor the potency of these compounds as antiestrogens. Indeed, compounds with high affinity for the estrogen receptor and greatest antiestrogenic potency have low affinities for these antiestrogen binding sites. Antiestrogenic potency correlates best with estrogen receptor affinity and not with affinity for antiestrogen binding sites. In summary, our findings suggested that interaction with the estrogen receptor is most likely the mechanism through which antiestrogens evoke their growth inhibitory effects.
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약학대학 > 약학과 > Journal papers
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