Effects of Hormones and Growth Factors on the Growth of Six Human Breast Cancer Cell Lines in Defined Media1

Küng, Willy; Silber, E.; Novak, Ilse; Eppenberger, Urs

doi:10.1159/000412799

Cited by 13 publications

(1 citation statement)

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“…It is possible that the MCF-7 cells used represent 2 different sublines. In support of this view is the demonstration of different responsiveness of the cells to estradiol when assessed for mitogenicity: while the cells of the Dutch group were only slightly stimulated, estradiol was always a potent mitogen for our MCF-7 cells in the presence or absence of dextran-charcoal-treated FCS (Roos et al, 1983;Kung et al, 1986Kung et al, , 1989). However, the very different results in c-fos-mRNA-induction by estradiol obtained with the 2 puta- tive MCF-7 sublines is striking because they indicate that there is only a loose correlation, if any, between mitogenic response and proto-oncogene activation.…”

Section: Discussionmentioning

confidence: 65%

Inhibition of growth‐factor‐activated proliferation by anti‐estrogens and effects on early gene expression of mcf‐7 cells

Wosikowski

Küng

Hasmann

et al. 1993

Intl Journal of Cancer

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Recently, it was reported that the anti-estrogen tamoxifen not only inhibits estradiol-stimulated growth of MCF-7 cells but also significantly reduces the proliferation rate of cells stimulated by growth factors. We have confirmed this finding and also shown that the new anti-estrogen droloxifene inhibits the proliferation of epidermal growth factor (EGF) and insulin-like growth factor-I (IGF-I)-stimulated MCF-7 cells. The growth-factor-induced proliferation was inhibited in a dose-dependent manner by the anti-estrogens in the complete absence of estrogen and FCS. Of the anti-estrogens, droloxifene was considerably more potent than tamoxifen. Because the expression of the proto-oncogenes c-fos and c-myc has been considered a key event in development of the mitogenic response, we examined the effects of anti-estrogens on c-myc and c-fos gene expression. We included in these investigations the steroidal anti-estrogen ICI 164,384 because this compound has no or very little estrogenic activity. The studies revealed that all 3 anti-estrogens transiently induced c-myc mRNA expression. However, the anti-estrogens inhibited estradiol-induced c-myc mRNA expression, although with different potencies. Pre-incubation of MCF-7 cells with droloxifene and tamoxifen resulted in elevated levels of growth-factor-induced c-myc mRNA expression. In contrast, the anti-estrogens did not induce c-fos mRNA or affect the expression of c-fos mRNA induced by growth factors. In conclusion, non-steroidal anti-estrogens inhibit growth-factor-stimulated proliferation of MCF-7 cells without inhibiting growth-factor-induced c-myc or c-fos mRNA expression.

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Section: Discussionmentioning

confidence: 65%

Inhibition of growth‐factor‐activated proliferation by anti‐estrogens and effects on early gene expression of mcf‐7 cells

Wosikowski

Küng

Hasmann

et al. 1993

Intl Journal of Cancer

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Increased expression of estrogen-receptor exon-5-deletion variant in relapse tissues of human breast cancer

et al. 1998

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DNA synthesis in estrogen receptor-positive human breast cancer takes place preferentially in estrogen receptor-negative cells

Ballaré¹,

Bravo²,

Laucella³

et al. 1989

Cancer

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The primary breast tumors of 27 patients were analyzed for the expression of estrogen receptors (ER) and DNA synthesis. Seventeen tumors were ER-positive, and the simultaneous expression of ER and DNA synthesis could be analyzed in 14 ER-positive tumors. DNA synthesis was measured through the thymidine labeling index (TLI). ER expression was detected by immunohistochemistry with monoclonal antibodies. In these tumors, 38.6% +/- 13.1% of the cells were ER-positive (average TLI = 0.60% +/- 0.70%), as opposed to the presence of 61.4% +/- 13.1% of ER-negative cells (average TLI = 0.65% +/- 0.53%). In 12 of 14 tumors, both ER-positive and ER-negative cells were found to be engaged in DNA synthesis, whereas in two tumors only ER-negative cells were synthesizing DNA. On the basis of the TLI and the proportion of ER-negative and ER-positive cells in the total population, it is suggested that the ER-positive and ER-negative compartments are interrelated in most tumors. In five tumors, the ER-negative compartment would be a precursor of the ER-positive segment, whereas in six tumors the ER-positive segment appears to be a precursor of the ER-negative one. In three tumors, no evidence of an interrelationship between both segments could be found. In the 14 tumors analyzed, it also was found that 69.1% +/- 21.3% of the DNA-synthesizing cells were ER-negative; this probably accounts for the temporary remissions observed after hormonal treatment in breast cancer.

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Effects of Hormones and Growth Factors on the Growth of Six Human Breast Cancer Cell Lines in Defined Media1

Cited by 13 publications

References 0 publications

Inhibition of growth‐factor‐activated proliferation by anti‐estrogens and effects on early gene expression of mcf‐7 cells

Inhibition of growth‐factor‐activated proliferation by anti‐estrogens and effects on early gene expression of mcf‐7 cells

Increased expression of estrogen-receptor exon-5-deletion variant in relapse tissues of human breast cancer

DNA synthesis in estrogen receptor-positive human breast cancer takes place preferentially in estrogen receptor-negative cells

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