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首页> 外文期刊>Journal of Cellular Physiology >The high-mobility group A1-estrogen receptor β nuclear interaction is impaired in human testicular seminomas
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The high-mobility group A1-estrogen receptor β nuclear interaction is impaired in human testicular seminomas

机译：高机动组A1-estrogen受体β人类的核相互作用受损睾丸精原细胞瘤

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It is well established that estrogens participate in the control of normal spermatogenesis and endogenous or environmental estrogens are involved in pathological germ cell proliferation including testicular germ cell tumors. The effects of estrogen are now known to be mediated by estrogen receptor-α (ERα) and ERβ subtypes, but only ERβ has been found in human germ cells of normal testis. However, its expression was markedly diminished in human testicular seminomas. The expression and the possible interaction of ERβ and HMGA1 were studied in normal germ cells and in human testicular seminomas. GC1 and TCam-2 germ cell lines, were used; in addition, a tissue micro-array (TMA) was built using the most representative areas from 35 cases of human testicular seminomas. The expression and the interaction of ERβ and HMGA1 were observed by using immunoprecipitation and Western blot analyses in combination with immunocytochemistry and immunofluorescence analyses. Here, we show that ERβ interacts with HMGA1 in normal germ cells, while down regulation of ERβ associates with transcriptional co-regulator HMGA1 over-expression and cytoplasmic localization both in human testicular seminomas and in TCam-2 cell line. In addition, we show that 17β-oestradiol induces an HMGA1 increased cytoplasmic expression associated to an ERβ down-regulation in TCam-2 cell line. Taken together, our results suggest that exposure to estrogens or estrogen-mimics, in some as of yet undefined manner, diminishes the ERβ-mediated growth restraint in human testicular seminoma, probably due to the HMGA1 cytoplasmic delocalization associated with ERβ down-regulation.
机译：证实雌激素参与正常的精子发生和控制的内源性或环境雌激素参与病理生殖细胞增殖包括睾丸生殖细胞肿瘤。影响雌激素目前已知是介导的雌激素受体-α(ERα)和ERβ亚型,但只有在人类生殖细胞ERβ被发现正常的睾丸。在人类睾丸明显减弱精原细胞瘤。交互ERβ和HMGA1进行了研究正常的生殖细胞和人类睾丸精原细胞瘤。使用;使用最具代表性的地区从35人类睾丸精原细胞瘤的病例。表达和ERβ和HMGA1的交互观察通过免疫沉淀反应和免疫印迹分析结合免疫细胞化学和免疫荧光分析。HMGA1在正常的生殖细胞,而监管ERβassociates的转录co-regulator HMGA1表达和细胞质定位在人类的睾丸精原细胞瘤和TCam-2细胞系。我们表明,17β雌二醇诱发HMGA1增加细胞质表达相关的ERβ下调TCam-2细胞系。在一起,我们的研究结果表明,接触在一些的雌激素或estrogen-mimics,未定义的方式,减少了ERβ介导增长的约束人类睾丸精原细胞瘤,可能由于HMGA1细胞质移位与ERβ相关联下调。

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