Control of mammary epithelial cell DNA synthesis by epidermal growth factor, cholera toxin, and IGF-1: specific inhibitory effect of prolactin on EGF-stimulated cell growth.

Control of mammary epithelial cell DNA synthesis by epidermal growth factor, cholera toxin, and IGF-1: specific inhibitory effect of prolactin on EGF-stimulated cell growth.
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表皮生长因子、霍乱毒素和 IGF-1 对乳腺上皮细胞 DNA 合成的控制:催乳素对 EGF 刺激的细胞生长的特异性抑制作用。

DOI:
10.1006/excr.1994.1015
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发表时间:
1994
影响因子:
3.7
通讯作者:
Sheffield,LG
Sheffield,LG
中科院分区:
医学3区
文献类型:
--
作者:
Fenton,SE;Sheffield,LG

文献摘要

被引文献

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表皮生长因子(EGF)在体内刺激小鼠乳腺细胞增殖,但其在乳腺中的最高水平是在泌乳中期,此时乳腺生长很少。本研究使用正常小鼠乳腺上皮细胞系(NMuMG)来确定乳腺分裂原EGF、霍乱毒素(CT)和胰岛素样生长因子-1 (IGF-1)对细胞增殖的影响,以及添加泌乳激素(PRL)如何改变细胞生长。与基础水平相比,EGF和CT刺激NMuMG细胞的DNA合成增加了四倍以上。当细胞用IGF-1处理时,只观察到DNA合成的双重刺激。当这些药物与其他药物联合使用时,s期细胞的百分比略有增加。生理水平的PRL对CT或igf -1诱导的DNA合成没有显著影响,但将egf刺激的细胞增殖降低到基础水平。此外,在EGF存在的情况下,PRL将s期细胞的百分比降低到IGF-1和ct诱导的水平。有趣的是,PRL在处理2小时后增加了EGF mRNA的细胞水平,这与乳原激素培养的小鼠乳腺的反应相似。我们得出结论,尽管PRL可以增加乳腺上皮细胞中EGF mRNA的数量,但它也可以消除EGF诱导的有丝分裂。
Epidermal growth factor (EGF) stimulates mouse mammary cell proliferationin vivo, but its maximal level in the mammary gland is at midlactation, when little mammary growth takes place. The present studies use a normal murine mammary gland epithelial cell line (NMuMG) to determine the effects of the mammary mitogens EGF, cholera toxin (CT), and insulin-like growth factor-1 (IGF-1) on cell proliferation and how cell growth is altered by addition of the lactogenic hormone prolactin (PRL). EGF and CT stimulated over a fourfold increase of DNA synthesis in NMuMG cells when compared to basal levels. Only a twofold stimulation of DNA synthesis was observed when cells were treated with IGF-1. There was a slight increase in the percentage of cells in S-phase when these agents were added in combination with each other. Physiological levels of PRL had no significant effect on CT- or IGF-1-induced DNA synthesis but reduced EGF-stimulated cell proliferation to basal levels. Furthermore, PRL reduced the percentage of cells in S-phase to IGF-1- and CT-induced levels in the presence of EGF. Interestingly, PRL increased cellular levels of EGF mRNA after 2 h of treatment, which is similar to the response of mouse mammary glands cultured in lactogenic hormones. We conclude that even though PRL can increase the amount of EGF mRNA in mammary epithelial cells, it also eliminates EGF-induced mitogenesis.