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首页> 外文期刊>Molecular and Cellular Biology >Epidermal growth factor receptor, but not c-erbB-2, activation prevents lactogenic hormone induction of the beta-casein gene in mouse mammary epithelial cells.
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Epidermal growth factor receptor, but not c-erbB-2, activation prevents lactogenic hormone induction of the beta-casein gene in mouse mammary epithelial cells.

机译：表皮生长因子受体而不是c-erbB-2的活化阻止了小鼠乳腺上皮细胞中β-酪蛋白基因的促乳激素诱导。

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The HC11 cell line was isolated from mammary gland cells of pregnant mice. The cells displayed a normal phenotype and retained some characteristics of mammary epithelial cell differentiation. After treatment with the lactogenic hormones prolactin and glucocorticoids, the HC11 cells expressed the milk protein beta-casein. Various oncogenes were transfected and expressed in HC11 cells. The oncogenes were tested for their transformation ability and for their effects upon the differentiation of the HC11 cells. All of the oncogenes tested, including activated human Ha-ras, human transforming growth factor-alpha, activated rat neuT, and human c-erbB-2 activated by a point mutation in the transmembrane domain, caused transformation of the HC11 cells, as shown by tumor formation in nude mice. HC11 cells expressing the neuT and activated c-erbB-2 genes synthesized beta-casein in response to lactogenic hormones, whereas those expressing the Ha-ras or transforming growth factor-alpha oncogenes were no longer able to respond to the lactogenic hormones. This inhibition of beta-casein production occurs at the transcriptional level and in the transforming growth factor-alpha-transformed cells is due to an autocrine mechanism involving the activation of the epidermal growth factor receptor. This suggests that, although the c-erbB-2 and epidermal growth factor receptors are structurally quite similar, their activation has different effects upon mammary epithelial cell differentiation.
机译：从怀孕小鼠的乳腺细胞分离出HC11细胞系。这些细胞表现出正常的表型，并保留了乳腺上皮细胞分化的一些特征。用催乳激素催乳激素和糖皮质激素治疗后，HC11细胞表达了乳蛋白β-酪蛋白。各种致癌基因被转染并在HC11细胞中表达。测试了癌基因的转化能力以及它们对HC11细胞分化的影响。如图所示，所有测试的致癌基因，包括活化的人类Ha-ras，人类转化生长因子-α，活化的大鼠neuT和通过跨膜结构域中的点突变活化的人类c-erbB-2，均导致HC11细胞转化。裸鼠体内肿瘤的形成。表达neuT和激活的c-erbB-2基因的HC11细胞响应乳激素而合成了β-酪蛋白，而表达Ha-ras或转化生长因子-α癌基因的HC11细胞不再能够响应乳激素。 β-酪蛋白产生的这种抑制作用发生在转录水平，并且在转化生长因子-α转化的细胞中归因于涉及表皮生长因子受体活化的自分泌机制。这表明，尽管c-erbB-2和表皮生长因子受体在结构上非常相似，但它们的激活对乳腺上皮细胞分化有不同的影响。

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