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

Michelle J. Stanley, Michael W. Stanley, Ralph D. Sanderson, Richard Zera

Research output: Contribution to journalArticlepeer-review

117 Scopus citations

Abstract

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.

Original languageEnglish (US)
Pages (from-to)377-383
Number of pages7
JournalAmerican journal of clinical pathology
Volume112
Issue number3
DOIs
StatePublished - 1999

Keywords

  • Breast
  • Carcinoma
  • Fibroadenoma
  • Invasion
  • Proteoglycan
  • Stroma
  • Syndecan

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