Melanotransferrin gene expression in melanoma cells is correlated with high levels of Jun/Fos family transcripts and with the presence of a specific AP1-dependent ternary complex.

Melanotransferrin gene expression in melanoma cells is correlated with high levels of Jun/Fos family transcripts and with the presence of a specific AP1-dependent ternary complex.
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黑色素瘤细胞中的黑色转铁蛋白基因表达与高水平的 Jun/Fos 家族转录物以及特定的 AP1 依赖性三元复合物的存在相关。

DOI:
10.1042/bj3180883
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发表时间:
1996
期刊:
The Biochemical journal
影响因子:
--
通讯作者:
N. Duchange
N. Duchange
中科院分区:
--
文献类型:
--
作者:
A. Roze;M. L. Houbiguian;C. Debacker;M. Zakin;N. Duchange

文献摘要

被引文献

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转录因子AP 1参与黑素转铁蛋白(MTF)基因表达的调节进行了研究。MTF,也称为p97,是一种肿瘤相关抗原,在大多数黑色素瘤中过度产生。它的基因表达受一个含有两个AP 1结合位点的增强子元件的控制。通过北方分析,我们表明,MTf mRNA检测在不同水平的黑色素瘤SK-MEL-28细胞,其最大的表达与大量的Jun和Fos转录本的存在相一致。凝胶阻滞试验表明,诱导这些原癌基因的表达与增加的AP 1结合活性和MTF增强子的区域参与形成的三元AP 1依赖性复合物,暗示第二个核因子,其结合特性是类似的活化T细胞的核因子(NF-AT)。在瞬时表达实验中,由三元复合物形成产生的活性高且对黑素瘤细胞具有特异性。这些数据提供了一个可能的解释的机制,AP 1因子家族参与的MTF在黑色素瘤细胞的上调。
The involvement of the transcription factor AP1 in the regulation of melanotransferrin (MTf) gene expression was investigated. MTf, also known as p97, is a tumour-associated antigen that is overproduced in most melanomas. Its gene expression is under the control of an enhancer element containing two AP1 binding sites. By Northern analysis, we demonstrate that MTf mRNA is detected at various levels in melanoma SK-MEL-28 cells and that its greatest expression coincides with the presence of large amounts of jun and fos transcripts. Gel retardation assays revealed that the induction of expression of these proto-oncogenes is correlated with increased AP1 binding activity and that a region of the MTf enhancer is involved in the formation of a ternary AP1-dependent complex, implicating a second nuclear factor whose binding characteristics are similar to those of nuclear factor of activated T cells (NF-AT). In transient expression experiments, the activity resulting from ternary complex formation was high and specific to melanoma cells. These data provide a possible explanation for the mechanisms of AP1 factor family involvement in MTf up-regulation in melanoma cells.