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J C Faye

Publications and source records attributed to J C Faye.

At least 55 records · Page 3Linked to original sources

Antiestrogens, different sites of action than the estrogen receptor?

Nonsteroidal antiestrogens display antagonistic as well as agonistic properties when compared with estrogens. These observations and studies of their molecular interactions suggest that part of their activity is mediated through estrogen receptor (ER)-mediated pathways. However, other data, concerning mainly effects on growth and cellular proliferation, cannot be explained on this basis. Recent investigations have shown binding of these molecules to a number of other intracellular binding sites beside ER. Using different cell variants of the human breast cancer cell line MCF-7 we could confirm the peculiar role of one of these sites, the specific antiestrogen-binding site (ABS). Published data on ABS are critically reviewed.

Animals↗

Characterization of estrogen binding sites in the liver of the newt Pleurodeles waltl (Urodela:Amphibia): demonstration of a sex-linked heterogeneity.

Saturation analysis over a wide range of [3H]estradiol-17 beta concentrations (1-40 nM) in cytosols prepared from liver of the newt Pleurodeles waltl of both sexes revealed a sex-linked heterogeneity of the estradiol-17 beta binding sites. In females, one type of binding site has been identified as a classical receptor. It exhibited a high affinity for estradiol-17 beta (Kd = 9 X 10(-9) M), had a high specificity for estrogenic compounds and was stabilized by monothioglycerol. In males, in addition to the receptor found in females, a second estrogen binding component was detected, not observed in female cytosols. It exhibited a Kd of 4.8 X 10(-8) M for estradiol 17 beta, higher capacity and displayed the same highly specific estrogen binding as does the estrogen receptor. It was affected by monothioglycerol and its binding was found to be significantly increased on cytosol dilution, as well as by estrogen-treatment.

Animals↗

Different interaction of estradiol and antiestrogens with the estrogen receptor of rat uterus.

Cytosoluble estradiol-receptor (ER) complexes obtained from uteri of castrated rats show a 4.3 S sedimentation coefficient when analysed by sucrose gradient in high salt buffer both in the absence and presence of 0.1 M ammonium thiocyanate. After incubation with nuclei, the complexes sediment at 4.3 S and at 3.2 S, in the absence and presence of 0.1 M ammonium thiocyanate respectively. This structural modification of ER is also confirmed by gel filtration analysis. In similar conditions hydroxytamoxifen-ER complexes apparently do not undergo such a modification. However, increasing the molarity of the chaotropic ion up to 0.5 M shows that, in fact, the modification occurs. Sodium dodecylsulfate-polyacrylamide gel electrophoresis analysis of covalently linked tamoxifen aziridine-ER 'complexes' confirms that the nuclear treatment reduces the apparent molecular weight of ER from 62 000 to 47 000. These data demonstrate that, in vitro, nuclear ER is cleaved into a smaller molecular form and that the receptor fragments can be held together by the triphenylethylene antiestrogen hydroxytamoxifen.

Animals↗

Dissimilarities between the uterine estrogen receptor in cytosol of castrated and estradiol-treated rats.

The estrogen receptor (ER) in its native state appears oligomeric and can be dissociated by salt into a monomer with a mol wt of 50,000-80,000. Lower molecular weight fragments have also been observed but are considered to result from ER proteolysis by tissue proteases. Three-month-old Sprague-Dawley rats have been studied after castration, estradiol treatment (3 days at 25 micrograms/day), or during the normal estrus cycle. The uterine cytosol was labeled with [3H]estradiol, and the [3H]estradiol-receptor complexes were studied by sucrose gradient centrifugation, gel filtration, diethylaminoethyl (DEAE)-Trisacryl and phosphocellulose chromatography, and kinetic experiments. In low salt buffer in presence of molybdate (20 mM), uterine ER of castrated and treated rats could not be differentiated by sucrose gradient centrifugation (9.9S), gel filtration (7.7 nm), or DEAE-Trisacryl and phosphocellulose chromatography, but the dissociation rate at 23 C was lower for castrated than for treated rats (t1/2 = 45 and 27 min, respectively). In high salt buffer (0.4 M KCl) in presence of molybdate (20 mM), no difference was apparent by sucrose gradient centrifugation (3.7S) or gel filtration (3.4 nm), but again the dissociation rate at 23 C was lower for castrated than for treated rats (t1/2 = 102 and 45 min, respectively). In high salt buffer in presence of molybdate and ammonium thiocyanate (0.5 M), differences were observed by sucrose gradient centrifugation (3.6 and 3.2S), gel filtration (3.2 and 2.6 nm), and dissociation rate assays at 10 C (t1/2 = 24 and 12 min) for castrated and treated rats. The calculated wts were 50,000 and 35,000, respectively. Protection from limited proteolysis by molybdate, contained in all buffers used, plus various protease inhibitors, particularly leupeptin, as well as mixing tissues before homogenization, suggested that the 35,000-dalton monomer was not a product of protease action formed after cell breakage. ERs covalently labeled with [3H]tamoxifen aziridine also showed different entities of 62,000 and 47,000 mol wts, respectively, on denaturing polyacrylamide gels. In vitro activation and transformation were demonstrated for the two types of [3H]estradiol-receptor complexes by sucrose gradient centrifugation analysis and affinity for phosphocellulose and purified nuclei. Finally, it has been shown that both entities coexisted in different proportions during the diestrous (1:2) and proestrous (1:1) phases of the estrus cycle; only the low mol wt component was present during the estrous phase.

Animals↗

Interaction of estradiol and high density lipoproteins on proliferation of the human breast cancer cell line MCF-7 adapted to grow in serum free conditions.

The responsiveness of the human mammary carcinoma cell line MCF-7 to estradiol and tamoxifen treatment has been studied in different culture conditions. Cells from exponentially growing cultures were compared with cells in their initial cycles after replating from confluent cultures ("confluent-log" cells). It has been observed that estradiol stimulation of tritiated thymidine incorporation decreases with cell density and that "confluent-log" cells are estrogen unresponsive for a period of four cell cycles in serum-free medium conditions. On the other hand, growth of cells replated from exponentially growing, as well as from confluent cultures, can be inhibited by tamoxifen or a combined treatment with tamoxifen and the progestin levonorgestrel. This growth inhibitory effect can be rescued by estradiol when cells are replated from exponentially growing cultures. The growth inhibitory effect cannot be rescued by estradiol alone (10(-10) to 10(-8) M) when cells are replated from confluent cultures. In this condition, the addition of steroid depleted serum is necessary to reverse the state of estradiol unresponsiveness. Serum can be replaced by high density lipoproteins but not by low density lipoproteins or lipoprotein deficient serum. The present data show that estradiol and HDL interact in the control of MCF-7 cell proliferation.

Breast Neoplasms↗

Physicochemical and genetic evidence for specific antiestrogen binding sites.

In rat uterus and human breast cancer MCF-7 cell cytosol, the antiestrogens tamoxifen (Tam) and 4-hydroxytamoxifen (OH-Tam) bind to "antiestrogen binding sites" (ABS), which do not bind estradiol (E). Demonstrated in total cytosol by binding studies with radioactive antiestrogens in the presence of a large concentration of E, ABS can be physically separated from E-binding estrogen receptor (ER) by removing the latter with an E-containing bioaffinity adsorbent or with heparin-Sepharose gel. ABS concentration is 10-20% of that of ER; the Kd for Tam and OH-Tam is 1-2 x 10(-9) M, whereas the Kd of OH-Tam binding by ER (approximately equal to 1 x 10(-10) M) is approximately equal to 1/50 that of Tam. Other triphenylethylene antiestrogens compete against Tam for binding to ABS, contrary to steroid hormones. Sucrose gradient ultracentrifugation analyses of total cytosol and of affinity gel effluents show a heterogenous pattern of ABS from 10 to 40 S, unchanged by 0.4 M KCl and limited trypsinization (which however provoke transitions of ER from 8S to 4S forms) and by 20 mM molybdate (which stabilizes the 8S form of ER and prevents large aggregates). Preliminary results suggest that ABS may be associated with particulate components of the cell. RTx6 cells of a clone selected from MCF-7 cells for resistance to the antigrowth effect of Tam have ER in the same concentration and have similar affinity for E and antiestrogens as do unselected MCF-7 cells. However, RTx6 cells have virtually no ABS detectable by binding and gradient ultracentrifugation studies. It is proposed that the double binding of Tam and OH-Tam to ER and ABS in estrogen target cells may be related to the complex double series of estrogenic and "antiestrogenic" activities displayed by nonsteroidal triphenylethylene derivatives.

Animals↗