H�rtebestimmung in Wasser

Vignon, L.; Meunier, Louise; Marpmann, G.; Grünhut, L.; Giorgis, G.; Feliciani, G.; Carnevali, A.; Appelius, W.; Pfeifer, J.-P.; Wartha, V.; Monhaupt, M.; Drawe, P.; Procter, H. R.; Auerbach, Fr.; Basch, E.; Legler, L.; gasselin,; Grittner, A.; Winkler, L. W.

doi:10.1007/bf01306435

Cited by 3 publications

(4 citation statements)

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“…The secreted 52K-cath-D assayed in the same experiment was induced by antiestrogens in R27 cells but not in LY2 cells, in accordance with previous studies (18,26,27). The dissociated effects observed in LY2 cells, in which the antiestrogens induced the 2.2 kb mRNA but not the secreted 52K-cath-D is not yet explained, however they suggest an additional effect of antiestrogens on protein maturation and/or secretion.…”

Section: Effect Of Antiestrogens On Ncf7 Cells and Antiestrogenresistsupporting

confidence: 92%

“…2) The different effects of antiestrogens on the synthesis of the 2.2 kb-cath-D mRNA in antiestrogen-sensitive and -resistant cells confirm previous findings based on the quantification of secreted 52K-cath-D (18,26). The discrepancy observed in the LY2 subline, where antiestrogen stimulates mRNA-cathepsin D accumulation but not 52K-cath-D secretion (27) suggests an additional level of regulation for secretion.…”

Section: Discussionsupporting

confidence: 81%

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Estrogens and growth factors induce the mRNA of the 52K-pro-cathepsin-D secreted by breast cancer cells

et al. 1988

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The estrogen-induced 52K protein secreted by human breast cancer cells is a lysosomal protease recently identified as a pro-cathepsin D by sequencing several cDNA clones isolated from MCF7 cells (Augereau et al., Mol. Endocr.). Using one of these clones, we detected, in MCF7 cells, a 2.2 kb mRNA whose level was rapidly increased 4- to 10-fold by estradiol, but not by other classes of steroids. Other mitogens, such as epidermal growth factor and insulin, also induced the 2.2 kb mRNA in a dose-dependent manner. Induction with epidermal growth factor was as rapid but was 2- to 3-fold lower than with estradiol. Antiestrogens had no effect on the 52K-cathepsin-D mRNA in MCF7 cells, but became estrogen agonists in two antiestrogen-resistant sublines R27 and LY2. The use of transcription and translation inhibitors and nuclear run-on experiments indicate that estradiol enhances transcription of the 52K-cathepsin-D gene in MCF7 cells.

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Section: Effect Of Antiestrogens On Ncf7 Cells and Antiestrogenresistsupporting

confidence: 92%

Section: Discussionsupporting

confidence: 81%

Estrogens and growth factors induce the mRNA of the 52K-pro-cathepsin-D secreted by breast cancer cells

et al. 1988

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“…The residual E2 was removed from CME2 prior to its use as a mitogen. This kind of result had also been obtained by Vignon and Rochefort and their colleagues [58], who had noticed that MCF-7 cells grew faster with less frequent medium exchanges as compared to cells in which medium was changed every other day. They had also noted that CME2 was directly capable of stimulating other MCF-7 cells.…”

Section: Growth Factor Production and Growth Regulation By Human Breasupporting

confidence: 71%

Growth regulation of human breast carcinoma occurs through regulated growth factor secretion

Lippman¹,

Dickson²,

Gelmann³

et al. 1987

J of Cellular Biochemistry

116

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We describe studies on human breast cancer in which it is shown that specific growth factors (IGF-I, TGF alpha, PDGF) are secreted by human breast cancer cells and likely to be involved in tumor growth and progression. These activities are regulated by estradiol in hormone-dependent breast cancer and secreted constitutively by hormone-independent cells. These growth factor activities can induce the growth of hormone-dependent cells in vivo in athymic nude mice. Hormone-dependent breast cancer cells also secrete TGF beta, a growth-inhibitory substance, when treated with antiestrogens. TGF beta functions as a negative autocrine growth regulator and is responsible for some of the growth-inhibitory effects of antiestrogens.

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“…We have investigated the ER system in the C3H mouse mammary carcinoma. This tumor is estrogen-unresponsive since in vivo estradiol is unable to increase the concentration of the progesterone receptor sites, and does not sustain tumor growth [3, 41. In this tumor, the ER is present at moderate concentrations (20 -40 fmol/mg cytosol protein) and, after estrogen binding, is translocated into the nucleus in vivo [3]. Therefore the estrogen-unresponsiveness of the tumor is not due to the absence of nuclear ER.…”

mentioning

confidence: 94%

A cytosol protease from the estrogen-resistant C3H mammary carcinoma increases the affinity of the estrogen receptor for DNA in vitro

Baskevitch

Rochefort

1985

Eur J Biochem

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We have previously shown, in the estrogen-unresponsive C3H mouse mammary tumor that the affinity of the estrogen receptor (ER) for calf thymus DNA in vitro is four-times higher than that of uterine ER [Baskevitch, P. P., Vignon, F., Bousquet, C. and Rochefort, H. (1983) Cancer Res. 43,22901. By mixing cytosols from this tumor and uterus, we describe a tumor factor capable of increasing ER affinity for DNA, as assayed by DNA-cellulose chromatography and saturation studies. The activity of this factor was inhibited by a-chymotrypsin-inhibitors such as N-tosylphenylalanylchloromethane and chymostatin. Using the fluorogenic substrate glutarylglycylglycylphenylalanyl-N-naphthylamide, we assayed such a protease in the C3H mammary tumor cytosol. This protease and the factor altering ER-DNA binding were eluted together from chromatography on DEAE-cellulose, AcA 44, and carboline-agarose and were sensitive to the same inhibitors. The partially purified factor decreases the molecular mass of the estrogen receptor as seen by denaturing electrophoresis after covalent labelling of the ER with [3H]tamoxifen aziridine. We suggest that the increase of ER affinity for DNA and the decrease of ER molecular size are due to the same protease with an a-chymotrypsin-like specificity.Systems resistant to steroid hormones are useful in analyzing the sequence of hormone action, particularly the nuclear and DNA binding of the receptor-hormone complex, and in determining their biological significance [I]. In mammary tumors, estrogen resistance is mostly associated with the lack of assayable estrogen receptor sites [2]. However, in humans, 50% of breast cancers which possess estrogen receptor (ER-positive) do not respond to endocrine therapy. One possibility is that the ER are present, and are capable of binding the hormone, but are unable to transduce the message efficiently to chromatin. In this respect, hormone-resistant and ER-positive experimental mammary tumors are particularly interesting.We have investigated the ER system in the C3H mouse mammary carcinoma. This tumor is estrogen-unresponsive since in vivo estradiol is unable to increase the concentration of the progesterone receptor sites, and does not sustain tumor growth [3, 41. In this tumor, the ER is present at moderate concentrations (20 -40 fmol/mg cytosol protein) and, after estrogen binding, is translocated into the nucleus in vivo [3]. Therefore the estrogen-unresponsiveness of the tumor is not due to the absence of nuclear ER. It may therefore be the consequence of a post-receptor defect [5]. We have recently shown that the ER from C3H tumor has a fourfold higher affinity in vitro for non-specific DNA as compared to the ER

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H�rtebestimmung in Wasser

Cited by 3 publications

References 0 publications

Estrogens and growth factors induce the mRNA of the 52K-pro-cathepsin-D secreted by breast cancer cells

Estrogens and growth factors induce the mRNA of the 52K-pro-cathepsin-D secreted by breast cancer cells

Growth regulation of human breast carcinoma occurs through regulated growth factor secretion

A cytosol protease from the estrogen-resistant C3H mammary carcinoma increases the affinity of the estrogen receptor for DNA in vitro

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