Constitutive and Regulated Secretion of Epidermal Growth Factor and Transforming Growth Factor-β1 in MDA-MB-231 Breast Cancer Cell Line in 11-Day Cultures

1999 ◽  
Vol 11 (10) ◽  
pp. 753-757 ◽  
Author(s):  
Pere A Martı́nez-Carpio ◽  
Cristina Mur ◽  
Pilar Rosel ◽  
Miguel A Navarro
Keyword(s):  
Breast Cancer ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Cell Line ◽  
Breast Cancer Cell Line ◽  
Transforming Growth Factor ◽  
Cancer Cell Line ◽  
Transforming Growth Factor Β1 ◽  
Regulated Secretion ◽  
Epidermal Growth

scholarly journals Epidermal growth factor receptor gene-amplified MDA-468 breast cancer cell line and its nonamplified variants.

1987 ◽  
Vol 7 (1) ◽  
pp. 251-257 ◽  
Author(s):  
J Filmus ◽  
J M Trent ◽  
M N Pollak ◽  
R N Buick
Keyword(s):  
Breast Cancer ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Cell Line ◽  
Breast Cancer Cell Line ◽  
Egf Receptor ◽  
Receptor Gene ◽  
Cancer Cell Line ◽  
Egf Receptors ◽  
Epidermal Growth

We have recently reported (J. Filmus, M. N. Pollak, R. Cailleau, and R. N. Buick, Biochem. Biophys. Res. Commun. 128:898-905, 1985) that MDA-468, a human breast cancer cell line with a high number of epidermal growth factor (EGF) receptors, has an amplified EGF receptor gene and is growth inhibited in vitro pharmacological doses of EGF. We have derived several MDA-468 clonal variants which are resistant to EGF-induced growth inhibition. These clones had a number of EGF receptors, similar to normal human fibroblasts, and had lost the EGF receptor gene amplification. Karyotype analysis showed that MDA-468 cells had an abnormally banded region (ABR) in chromosome 7p which was not present in the variants. It was shown by in situ hybridization that the amplified EGF receptor sequences were located in that chromosome, 7pABR. Five of the six variants studied were able to generate tumors in nude mice, but their growth rate was significantly lower than that of tumors derived from the parental cell line. The variant that was unable to produce tumors was found to be uniquely dependent on EGF for growth in soft agar.

scholarly journals Epidermal growth factor receptor gene-amplified MDA-468 breast cancer cell line and its nonamplified variants

1987 ◽  
Vol 7 (1) ◽  
pp. 251-257
Author(s):  
J Filmus ◽  
J M Trent ◽  
M N Pollak ◽  
R N Buick
Keyword(s):  
Breast Cancer ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Cell Line ◽  
Breast Cancer Cell Line ◽  
Egf Receptor ◽  
Receptor Gene ◽  
Cancer Cell Line ◽  
Egf Receptors ◽  
Epidermal Growth

We have recently reported (J. Filmus, M. N. Pollak, R. Cailleau, and R. N. Buick, Biochem. Biophys. Res. Commun. 128:898-905, 1985) that MDA-468, a human breast cancer cell line with a high number of epidermal growth factor (EGF) receptors, has an amplified EGF receptor gene and is growth inhibited in vitro pharmacological doses of EGF. We have derived several MDA-468 clonal variants which are resistant to EGF-induced growth inhibition. These clones had a number of EGF receptors, similar to normal human fibroblasts, and had lost the EGF receptor gene amplification. Karyotype analysis showed that MDA-468 cells had an abnormally banded region (ABR) in chromosome 7p which was not present in the variants. It was shown by in situ hybridization that the amplified EGF receptor sequences were located in that chromosome, 7pABR. Five of the six variants studied were able to generate tumors in nude mice, but their growth rate was significantly lower than that of tumors derived from the parental cell line. The variant that was unable to produce tumors was found to be uniquely dependent on EGF for growth in soft agar.

Steroidal regulation of oestradiol-17β dehydrogenase activity of the human breast cancer cell line MCF-7

1988 ◽  
Vol 118 (1) ◽  
pp. 149-154 ◽  
Author(s):  
E. F. Adams ◽  
N. G. Coldham ◽  
V. H. T. James
Keyword(s):  
Breast Cancer ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Human Breast Cancer ◽  
Transforming Growth Factor ◽  
Cancer Cell Line ◽  
Human Breast Cancer Cell ◽  
Human Breast ◽  
Epidermal Growth ◽  
Mcf 7

ABSTRACT We have examined the direct effects of progestins, oestrogens, peptide hormones and growth factors on oestradiol-17β dehydrogenase (OE2DH) activity of cultures of the human breast cancer cell line MCF-7. Cells were cultured in the presence of steroid or peptide for 6 days, after which the number of cells was determined and cellular OE2DH activity assessed. Progesterone, 6α-methyl-17α-hydroxyprogesterone acetate, norethisterone and d(−)-norgestrel all profoundly inhibited cell mitosis and stimulated reductive (oestrone→oestradiol-17β) and oxidative (oestradiol-17β→oestrone) OE2DH activity. Both oestrone and oestradiol-17β directly stimulated reductive OE2DH activity, but had no effect on the oxidative direction. Oestradiol-17β stimulated cell growth only in phenolred free culture medium. Ovine prolactin, LH, epidermal growth factor and transforming growth factor did not alter OE2DH activity but small stimulatory effects on the growth of MCF-7 cells were exerted by prolactin and a combination of transforming growth factor with epidermal growth factor. It is concluded that these results may explain, at least in part, the alterations in mitotic activity and tissue oestradiol-17β levels observed in breast tissue during varying physiological and pathological conditions, such as during the menstrual cycle and in breast cancers. J. Endocr. (1988) 118, 149–154

The cytostatic effects of α-interferon may be mediated by transforming growth factor-β

1989 ◽  
Vol 2 (2) ◽  
pp. 131-136 ◽  
Author(s):  
D. J. Kerr ◽  
I. B. Pragnell ◽  
A. Sproul ◽  
S. Cowan ◽  
T. Murray ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Growth Factor ◽  
Cell Line ◽  
Breast Cancer Cell Line ◽  
Human Breast Cancer ◽  
Transforming Growth Factor ◽  
Cancer Cell Line ◽  
Transforming Growth Factor Β ◽  
Human Breast Cancer Cell ◽  
Human Breast

ABSTRACT There is some evidence to suggest that transforming growth factor-β (TGF-β) mediates the cytostatic effects of the anti-oestrogen tamoxifen. In this study we have demonstrated that α-interferon has a significant anti-proliferative effect on the oestrogen receptor-positive human breast cancer cell line ZR-75. There is decreased phenotypic expression of the oestrogen receptors (to about 30% of control values) and increased TGF-β mRNA. Under the growth conditions used here, ZR-75 cells had approximately 5800 TGF-β binding sites per cell, with an apparent dissociation constant of 70 pm, and we have shown that the anti-proliferative effects of α-interferon can be reduced by 60% by co-treating the cells with a TGF-β polyclonal antibody. The cytostatic effects of α-interferon may therefore be mediated by TGF-β in this human breast cancer cell line.

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