Syndecan-1 expression is induced in the stroma of infiltrating breast carcinoma.
Syndecan-1 expression is induced in the stroma of infiltrating breast carcinoma.
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DOI：
10.1093/ajcp/112.3.377
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发表时间：
1999-09
影响因子：
3.5
通讯作者：
M. J. Stanley;M. Stanley;R. Sanderson;R. Zera
中科院分区：
文献类型：
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作者：
M. J. Stanley;M. Stanley;R. Sanderson;R. Zera
硫酸乙酰肝素蛋白聚糖多配体蛋白聚糖-1的表达缺失导致细胞粘附减少、侵袭潜力增加和体外乳腺上皮细胞生长失调。我们比较了syndecan-1表达在恶性和非恶性乳腺组织使用单克隆抗体B-B4的荧光化学。与正常乳腺（n = 14）和间质上皮肿瘤（n = 10）的导管上皮相比，浸润性导管癌（n = 20）内的恶性细胞上的syndecan-1染色大大减少，所述正常乳腺和间质上皮肿瘤两者的导管上皮表现出广泛的基底外侧上皮染色。令人惊讶的是，恶性和非恶性乳腺组织的比较也揭示了一个显着的差异syndecan-1的表达在间质隔室。在浸润性导管癌中，syndecan-1的强染色存在于结缔组织内和基质细胞表面上，而syndecan-1表达在正常乳腺和基质上皮肿瘤的基质中不存在。由于syndecan-1与肝素结合生长因子如FGF-2相互作用，syndecan-1在肿瘤间质内的积累可能有助于浸润性乳腺癌的广泛血管生成和间质增殖特征。此外，间质内syndecan-1的诱导，加上恶性细胞上syndecan-1的丢失，表明syndecan-1表达的变化在促进乳腺浸润性导管癌的转移表型中是至关重要的。
Loss of expression of the heparan sulfate proteoglycan syndecan-1 leads to reduced cell adhesion, increased invasive potential, and dysregulated growth of mammary epithelial cells in vitro. We compared syndecan-1 expression in malignant and nonmalignant breast tissues using immunohisto-chemistry with monoclonal antibody B-B4. Staining for syndecan-1 is greatly diminished on malignant cells within infiltrating ductal carcinomas (n = 20) as compared with ductal epithelium of both normal breast (n = 14) and stromal-epithelial neoplasms (n = 10), which exhibit extensive basolateral epithelial staining. Surprisingly, comparison of malignant and nonmalignant breast tissue also reveals a striking difference in expression of syndecan-1 within the stromal compartment. In infiltrating ductal carcinomas, strong staining for syndecan-1 is present both within the connective tissue and on stromal cell surfaces, whereas syndecan-1 expression is absent in the stroma of both normal breast and stromal-epithelial neoplasms. Because syndecan-1 interacts with heparin-binding growth factors such as FGF-2, accumulation of syndecan-1 within the tumor stroma may contribute to the extensive angiogenesis and stromal proliferation characteristic of infiltrating breast carcinoma. Moreover, the induction of syndecan-1 within the stroma, coupled with the loss of syndecan-1 on malignant cells, suggests that changes in syndecan-1 expression are critical in promoting the metastatic phenotype of infiltrating ductal carcinoma of the breast.