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二甲基亚砜和视黄酸对人卵巢腺癌细胞抗原模式影响的比较分析

Comparative analysis of the effects of dimethyl sulfoxide and retinoic acid on the antigenic pattern of human ovarian adenocarcinoma cells.

作者信息

Grunt T W, Somay C, Oeller H, Dittrich E, Dittrich C

机构信息

Department of Internal Medicine I, University of Vienna, Austria.

出版信息

J Cell Sci. 1992 Oct;103 ( Pt 2):501-9. doi: 10.1242/jcs.103.2.501.

Abstract

HOC-7 malignant ovarian surface epithelial cells have been exposed to differentiation promoters like dimethyl sulfoxide (DMSO) and retinoic acid (RA) and the resulting cell phenotypes were characterized immunologically. Immunocytochemistry revealed that DMSO caused elevation of membrane-associated staining for epidermal growth factor-receptor (EGF-R) and for desmoplakins I and II (DPI+II). DMSO also stimulated cytoplasmic and surface labelling for CA 125 and extracellular deposition of fibronectin (FN). A fixed-cell ELISA system was used for quantification of these differentiation-like responses and revealed that DMSO efficiently induced expression of EGF-R, CA 125, FN and DPI+II in dose-dependent manner. Immunocytochemistry, ELISA and Western blotting additionally demonstrated that both DMSO and RA caused down-regulation of myc oncoproteins. Densitometer evaluation of electrophoresed proteins revealed a 50% DMSO- and a 25% RA-induced myc reduction. Apart from growth reduction, which was seen for both inducers, inhibition of myc gene expression was the only response of HOC-7 cells to RA-treatment. The extent of myc down-regulation seems, therefore, to be crucial for the initiation of maturational processes in the cells. Subsequent phenotypic differentiation of HOC-7 cells causes elevated levels of EGF-R, CA 125, FN and DPI+II. This cell model might be useful for the distinction between induced growth reduction and differentiation of ovarian cancer cells.

摘要

将人卵巢癌表面上皮细胞系HOC - 7暴露于二甲基亚砜(DMSO)和视黄酸(RA)等分化促进剂中,并通过免疫方法对所产生的细胞表型进行表征。免疫细胞化学显示,DMSO导致表皮生长因子受体(EGF - R)以及桥粒斑蛋白Ⅰ和Ⅱ(DPI + Ⅱ)的膜相关染色增加。DMSO还刺激了CA 125的细胞质和表面标记以及纤连蛋白(FN)的细胞外沉积。使用固定细胞ELISA系统对这些类似分化的反应进行定量分析,结果表明DMSO能以剂量依赖方式有效诱导EGF - R、CA 125、FN和DPI + Ⅱ的表达。免疫细胞化学、ELISA和蛋白质印迹分析还表明,DMSO和RA均导致myc癌蛋白的下调。对电泳后的蛋白质进行光密度计评估显示,DMSO诱导myc减少50%,RA诱导减少25%。除了两种诱导剂均能导致细胞生长减缓外,抑制myc基因表达是HOC - 7细胞对RA处理的唯一反应。因此,myc下调的程度似乎对细胞成熟过程的启动至关重要。HOC - 7细胞随后的表型分化导致EGF - R、CA 125、FN和DPI + Ⅱ水平升高。该细胞模型可能有助于区分诱导的卵巢癌细胞生长减缓与分化。

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