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首页> 外文期刊>Breast cancer research and treatment. >Sex hormone-induced mammary carcinogenesis in the female Noble rats: expression of bcl-2 and bax in hormonal mammary carcinogenesis.
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Sex hormone-induced mammary carcinogenesis in the female Noble rats: expression of bcl-2 and bax in hormonal mammary carcinogenesis.

机译：性激素诱导的雌性Noble大鼠乳腺癌变：荷尔蒙乳腺癌变中bcl-2和bax的表达。

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We have established a Noble rat model to explore the mechanisms of hormonal mammary carcinogenesis, in which the role of androgen in promoting mammary carcinogenesis was highlighted. We have also established that stromal-epithelial interactions may be responsible for the promotional effects of testosterone in mammary carcinogenesis. Based on these understandings, in the present study we examined the expression of Bcl-2 and Bax in pre-malignant mammary glands from rats treated with different protocols of sex hormones for 7 weeks as well as sex hormone induced mammary tumours. We observed that Bcl-2 was strongly expressed in most of mammary tumour cells, whereas weak or negative in adjacent normal or hyperplastic ductal structures. On the contrary, Bax immunoreactivity was weak in mammary tumour cells while strongly expressed in adjacent normal or hyperplastic ductal structures. More importantly, the results from comparative study of 'pre-malignant' glands further showed that when animals were treated with 17beta-oestradiol, the mammary epithelial cells expressed high levels of Bcl-2. The results from rats treated with testosterone, either alone or in combination with oestrogen, give rise to high levels of Bax expression in 'pre-malignant' mammary glands. These observations indicate that in 'pre-malignant' mammary glands, treatment with testosterone, either alone or in combination with 17beta-oestradiol, may induce high apoptotic activities. However, in fully developed mammary tumours, the apoptotic activities apparently decrease in tumour cells. TUNEL assay provides further data to support this conclusion. Our study, thus, suggests that androgens may play a promoting role in mammary carcinogenesis by upregulation of Bax expression and induction of high apoptotic activities in 'pre-malignant' stage, which would provide a selective pressure favouring the expansion of the initiated cells.
机译：我们建立了一个Noble大鼠模型来探讨激素性乳腺癌发生的机制，其中雄激素在促进乳腺癌发生中的作用得到了强调。我们还确定，基质-上皮相互作用可能是睾丸激素在乳癌发生中的促进作用。基于这些理解，在本研究中，我们检查了Bcl-2和Bax在用不同性激素方案治疗7周的大鼠的恶性前乳腺以及性激素诱发的乳腺肿瘤中的表达。我们观察到Bcl-2在大多数乳腺肿瘤细胞中强烈表达，而在相邻的正常或增生性导管结构中则弱或呈阴性。相反，Bax免疫反应性在乳腺肿瘤细胞中较弱，而在邻近的正常或增生性导管结构中则强烈表达。更重要的是，“恶性前”腺比较研究的结果进一步表明，当用17β-雌二醇治疗动物时，乳腺上皮细胞表达高水平的Bcl-2。单独或与雌​​激素联合使用睾丸激素治疗的大鼠的结果在“恶变前”的乳腺中引起高水平的Bax表达。这些观察结果表明，在“恶变前”的乳腺中，单独或与17β-雌二醇联合使用睾丸激素治疗可能诱导高凋亡活性。然而，在充分发展的乳腺肿瘤中，肿瘤细胞的凋亡活性明显降低。 TUNEL分析提供了进一步的数据来支持这一结论。因此，我们的研究表明，雄激素可能通过上调Bax表达并诱导“恶变前”阶段高凋亡活性而在乳癌发生中发挥促进作用，这将提供有利于起始细胞扩增的选择性压力。

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