The successive stages of breast cancer growth and dissemination depend on cell-autonomous factors and the communication between tumor cells and their surrounding cellular and extracellular matrix microenvironment. The cell surface heparan sulfate proteoglycan Syndecan-1 is dysregulated both in tumor cells and cells of the breast tumor stroma, indicating a potential role in the pathogenesis of this most frequent malignancy in women. Indeed, Syndecan-1 interacts with numerous ligands and receptors relevant to tumor progression, affecting processes as diverse as cancer stem cell function, cell proliferation, apoptosis, cell adhesion, migration and invasion, tumor angiogenesis, and leukocyte function in the tumor stroma. The present review summarizes the current understanding of breast carcinogenesis in correlation with their Syndecan-1 expression, involved mechanisms, and proposed therapeutic strategies against Syndecan-1-related malignancy.

乳腺癌生长和传播的连续阶段取决于细胞自主因素以及肿瘤细胞与其周围细胞和细胞外基质微环境之间的通讯。细胞表面硫酸乙酰肝素蛋白多糖 Syndecan-1 在肿瘤细胞和乳腺肿瘤基质细胞中均失调，表明在这种女性最常见恶性肿瘤的发病机制中具有潜在作用。事实上，Syndecan-1 与许多与肿瘤进展相关的配体和受体相互作用，影响多种过程，如癌症干细胞功能、细胞增殖、凋亡、细胞粘附、迁移和侵袭、肿瘤血管生成和肿瘤基质中的白细胞功能。本综述总结了目前对乳腺癌发生与其 Syndecan-1 表达相关的理解，