Syndecan-1 expression is induced in the stroma of infiltrating breast carcinoma

Loss of expression of the heparan sulfate proteoglycan syndecan-1 leads to reduced cell adhesion, increased invasive potential, and dysregulated growt h of mammary epithelial cells in vitro. We compared syndecan-1 expression i n malignant and nonmalignant breast tissues using immunohisto-chemistry wit h monoclonal antibody B-B4. Staining for syndecan-1 is greatly diminished o n malignant cells within infiltrating ductal carcinomas (n = 20) as compare d with ductal epithelium of both normal breast (n = 14) and stromal epithel ial neoplasms (n = 10), which exhibit extensive basolateral epithelial stai ning, Surprisingly, comparison of malignant and nonmalignant breast tissue also reveals a striking difference in expression of syndecan-1 within the s tromal 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 no rmal 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. Mor eover; the induction of syndecan-1 within the stroma, coupled with the loss of syndecan-1 on malignant cells, suggests that changes in syndecan-1 expr ession are critical in promoting the metastatic phenotype of infiltrating d uctal carcinoma of the breast.