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雌激素对乳腺肿瘤细胞系中HLA I类分子表达的上调作用。

Upmodulation by estrogen of HLA class I expression in breast tumor cell lines.

作者信息

Rodríguez F, Perán F, Garrido F, Ruiz-Cabello F

机构信息

Servicio de Análisis Clínicos e Inmunología, Hospital Virgen de las Nieves, Universidad de Granada, Spain.

出版信息

Immunogenetics. 1994;39(3):161-7. doi: 10.1007/BF00241256.

Abstract

The expression of major histocompatibility complex (MHC) class I antigens was studied in five breast carcinoma cell lines before and after treatment with 17-beta estradiol. Increased HLA class I antigen expression correlated with the presence of estrogen receptors. The modulation of expression appeared to be mediated by transcriptional mechanisms, as revealed by class I mRNA levels. To elucidate the basis of MHC class I upregulation, we examined transcriptional factor binding activity to the class I regulatory element (CRE). Our results showed that 17-beta estradiol induced increases in factor binding activity to the CRE II probe, and decreases to the CRE I probe. In addition, our results suggested that factors that bind the CRE I region may modulate the binding of CRE II. Binding to CRE II was significantly increased in extracts pretreated with a competitor that contained the CRE I sequence, and that bound NF-kB/kBF1. In addition, induction of NF-kB binding activity by the tumor necrosis factor was accompanied by a decrease in nuclear factors that bind to the CRE II region.

摘要

在五个乳腺癌细胞系中,研究了17-β雌二醇处理前后主要组织相容性复合体(MHC)I类抗原的表达情况。HLA I类抗原表达的增加与雌激素受体的存在相关。如I类mRNA水平所示,表达的调节似乎是由转录机制介导的。为了阐明MHC I类上调的基础,我们检测了转录因子与I类调节元件(CRE)的结合活性。我们的结果表明,17-β雌二醇诱导了与CRE II探针结合活性的增加,以及与CRE I探针结合活性的降低。此外,我们的结果表明,结合CRE I区域的因子可能调节CRE II的结合。在用包含CRE I序列且结合NF-kB/kBF1的竞争者预处理的提取物中,与CRE II的结合显著增加。此外,肿瘤坏死因子对NF-kB结合活性的诱导伴随着与CRE II区域结合的核因子的减少。

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