Estrogen Inhibits the Growth of MCF‐7 Cell Variants Resistant to Transforming Growth Factor‐beta

Hagino, Yoshiaki; Mawatari, Masasumi; Yoshimura, Akihiko; Kohno, Kimitoshi; Kobayashi, Michio; Kuwano, Michihiko

doi:10.1111/j.1349-7006.1988.tb00013.x

Cited by 9 publications

(10 citation statements)

References 15 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The dissociation constants for tamoxifen to the estradiol receptor were about 100 times lower than for LY117018 in both cell lines. Receptor content in ES-1 cells was 2-fold greater than in MCF-7 cells, which is consistent with our previous study (Hagino et al, 1988).…”

Section: Tamoxifen (Misupporting

confidence: 93%

“…ES-1 cells also induce 52-kDa protein, 160-kDa protein and pS2 protein mRNAs in the presence of estradiol (Hagino et al, 1988;Mizoguchi et al, 1990). The 67-kDa protein is also specifically induced in estradiol-treated ES-1 cells, and this protein includes t-PA (Mizoguchi et al, 1990).…”

Section: Discussionmentioning

confidence: 88%

“…The cells were grown in RPMI 1640 medium supplemented with sodium bicarbonate (2 g/l) porcine insulin and 10% (vlv) fetal bovine serum pretreated with dextran-coated charcoal to eliminate estrogens in serum (Hagino et al, 1988;Asoh et al, 1989).…”

Section: Cell Line and Cell Culturementioning

confidence: 99%

“…The human mammary carcinoma MCF-7 cell line and its variant ES-1 line have been previously described (Hagino et al, 1988;Mizoguchi et al, 1990). The cells were grown in RPMI 1640 medium supplemented with sodium bicarbonate (2 g/l) porcine insulin and 10% (vlv) fetal bovine serum pretreated with dextran-coated charcoal to eliminate estrogens in serum (Hagino et al, 1988;Asoh et al, 1989).…”

Section: Cell Line and Cell Culturementioning

confidence: 99%

“…Among the human PAS, u-PA (Mr of 54 kDa) and t-PA (Mr of 70 m a ) , MCF-7 cells produce t-PA but not u-PA (Ryan et al, 1984). We have isolated a mutant of MCF-7, ES-1, which is highly responsive to estrogen (Hagino et al, 1988). Treatment of ES-1 with estradiol induces much higher levels of t-PA than u-PA, but estradiol-treated MCF-7 cells cannot induce a significant amount of t-PA (Mizoguchi et al, 1990).…”

mentioning

confidence: 99%

See 4 more Smart Citations

Counteraction of estradiol‐induced activation of tissue‐type plasminogen activator in a human breast cancer cell line by an anti‐estrogen, LY117018

Uchiumi

Mizoguchi

Hagino

et al. 1991

Intl Journal of Cancer

View full text Add to dashboard Cite

LY117018 is a non-steroid anti-estrogen which exhibits about 100 times higher affinity for estrogen receptor than tamoxifen, another anti-estrogen. The cell line ES-1, which was isolated from human breast cancer MCF-7 cells, was highly sensitive to the cytocidal action of estradiol. Growth of ES-1 cells was inhibited by 10(-8)M 17 beta-estradiol, a concentration that stimulated the growth of parental MCF-7 cells. The estradiol-induced growth inhibition of ES-1 cells was almost completely reversed by treatment with LY117018, but not by treatment with tamoxifen. The relative binding affinity of LY117018 for estradiol receptor was equal to that of estradiol in both MCF-7 and ES-1 cells. Treatment of ES-1 cells with estradiol specifically induced tissue-type plasminogen activator (t-PA), whereas such estradiol-induced activation was not observed in parental MCF-7 cells. Quantitative immunoreactive assays and Northern blot analysis showed that estradiol-induced expression of t-PA was blocked by LY117018 in ES-1 cells. The inhibitory effect of tamoxifen was about 100 times lower than that of LY117018. The inhibition of t-PA gene expression by LY117018 might be due to competitive inhibition with estradiol in estradiol receptor binding.

show abstract

Section: Tamoxifen (Misupporting

confidence: 93%

Section: Discussionmentioning

confidence: 88%

Section: Cell Line and Cell Culturementioning

confidence: 99%

Section: Cell Line and Cell Culturementioning

confidence: 99%

mentioning

confidence: 99%

See 3 more Smart Citations

Counteraction of estradiol‐induced activation of tissue‐type plasminogen activator in a human breast cancer cell line by an anti‐estrogen, LY117018

Uchiumi

Mizoguchi

Hagino

et al. 1991

Intl Journal of Cancer

View full text Add to dashboard Cite

show abstract

A Computational Approach to Assess Breast Cancer Risk in Relation with Lifestyle Factors

Das¹,

Pradhan²,

Chatterjee³

et al. 2022

Biologically Inspired Techniques in Many Criteria Decision Making

View full text Add to dashboard Cite

Optimization of estrogen growth response in MCF-7 cells

Wiese

Kral

Dennis

et al. 1992

In Vitro Cell Dev Biol - Animal

View full text Add to dashboard Cite

The factors involved in estradiol-17 beta induced growth stimulation of MCF-7 human breast cancer cells have been examined. Wild type MCF-7 cells (and clone E3) were shown to undergo slow growth in phenol-red-free medium containing specific calf sera. The E3 clone was used to document a mean 6-day growth stimulation of 3.35-fold (doubling time = 33 +/- 3 h) in cultures supplemented with 10(-11) M estradiol-17 beta. The serum batch utilized in the culture medium is most important in acquiring significant growth stimulation of MCF-7 cells by estradiol-17 beta. Regardless of the absence of phenol-red, only selected sera (2 out of 14 tested) supported minimal growth of MCF-7 cells in the absence of added estradiol 17 beta (doubling time = 55 +/- 11 h). When a calf-serum-supplemented culture failed to display a complete growth response to estradiol-17 beta, it was due to the rapid growth of the cells in the control (minus estradiol-17 beta) flasks. Sera that promoted shorter doubling times for MCF-7 cells cultured in the absence of estradiol-17 beta were rendered less supportive of growth if treated with dextran-coated charcoal or when cultures were supplemented with the estrogen antagonist ICI 164,384 (10(-7) M). Pooled extracts of these sera were shown to contain stimulatory levels of estradiol-17 beta. Dextran-coated charcoal treatment of sera removed or deactivated factors (other than estradiol-17 beta) which were not only required for the growth of MCF-7 cells, but were necessary for estrogen-stimulated growth. Varying the serum-containing medium, buffer, and nutrient mix or the addition of insulin has no effect on the growth response of these cells to estradiol-17 beta. These investigations document the culture conditions required to produce a maximal and consistent proliferative effect of E2 on MCF-7 cells without exposing the serum constituent to damaging chemical or absorbent agents.

show abstract

Estrogen Inhibits the Growth of MCF‐7 Cell Variants Resistant to Transforming Growth Factor‐beta

Cited by 9 publications

References 15 publications

Counteraction of estradiol‐induced activation of tissue‐type plasminogen activator in a human breast cancer cell line by an anti‐estrogen, LY117018

Counteraction of estradiol‐induced activation of tissue‐type plasminogen activator in a human breast cancer cell line by an anti‐estrogen, LY117018

A Computational Approach to Assess Breast Cancer Risk in Relation with Lifestyle Factors

Optimization of estrogen growth response in MCF-7 cells

Contact Info

Product

Resources

About