Immunohistochemical study of syndecan-1 down-regulation and the expression of p53 protein or Ki-67 antigen in oral leukoplakia with or without epithelial dysplasia.
Immunohistochemical study of syndecan-1 down-regulation and the expression of p53 protein or Ki-67 antigen in oral leukoplakia with or without epithelial dysplasia.
复制标题
伴有或不伴有上皮不典型增生的口腔白斑中 syndecan-1 下调以及 p53 蛋白或 Ki-67 抗原表达的免疫组织化学研究。
DOI：
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发表时间：
2003
影响因子：
3.3
通讯作者：
Tetsu Takahashi
中科院分区：
文献类型：
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作者：
H. Kurokawa;Shinobu Matsumoto;T. Murata;Y. Yamashita;T. Tomoyose;Min Zhang;H. Fukuyama;Tetsu Takahashi
背景
白斑病是一种口腔癌前病变，有时会发展成鳞状细胞癌。因此，伴有上皮异常增生的白斑对于在细胞水平上研究致癌作用是有用的。本研究的目的是评估syndecan-1表达的丢失与p53蛋白和Ki-67抗原表达之间的潜在关联，并确定可靠的标记物用于预测口腔白斑伴上皮异型增生的恶性变化。
方法
应用免疫组化方法检测了43例口腔粘膜白斑伴或不伴上皮异常增生的组织中syndecan-1、p53和Ki-67的表达变化。受试者分为：无，13例;轻度异型增生，5例;中度异型增生，17例;重度异型增生，8例。同时检测了22例正常口腔上皮细胞中这些分子的表达。
结果
在正常上皮的角质形成细胞表面上观察到强烈的syndecan-1表达。随着上皮异型增生程度的增加，免疫阳性逐渐消失。p53和Ki-67在正常粘膜上皮中主要分布于基底细胞层，而在白斑中分布较广。具体而言，观察到的p53和Ki-67的标记指数在白斑上皮异型增生从轻度进展到中度或重度的显着变化。
结论
我们的研究结果表明，p53蛋白和Ki-67抗原的过度表达，以及syndecan-1在上皮下部的表达下调，与不典型增生的变化。因此，syndecan-1的表达下调可能是最重要的不典型增生变化的可靠标志。
BACKGROUND
Leukoplakia is an oral pre-cancerous lesion that sometimes develops into squamous cell carcinoma. Therefore, leukoplakia with epithelial dysplasia is useful for studying carcinogenesis at the cellular level. The purpose of this study was to evaluate a potential association between the loss of syndecan-1 expression and the expression of p53 protein and Ki-67 antigen, and to identify reliable markers for predicting malignant changes in oral leukoplakia with epithelial dysplasia.
METHODS
Changes in the expression of syndecan-1, p53, and Ki-67 were examined immunohistochemically in 43 cases of oral leukoplakia with or without epithelial dysplasia. The subjects were categorized as: none, 13 cases; mild dysplasia, 5 cases; moderate dysplasia, 17 cases; and severe dysplasia, 8 cases. The expression of these molecules in normal oral epithelia (22 cases) was also investigated.
RESULTS
Strong syndecan-1 expression was observed on the surface of keratinocytes in normal epithelium. Immunopositivity was lost gradually as the extent of epithelial dysplasia increased. In normal epithelium, p53 and Ki-67 appeared mainly in the basal cell layer, while they were more widely distributed in leukoplakia. Specifically, significant changes were observed in the labeling index of p53 and Ki-67 in leukoplakia as epithelial dysplasia progressed from mild to moderate or severe.
CONCLUSION
Our results reveal that overexpression of p53 protein and Ki-67 antigen, and down-regulation of syndecan-1 expression in the lower part of the epithelium, are associated with dysplastic changes. Therefore, the down-regulation of syndecan-1 expression may be the most important reliable marker for dysplastic changes.