摘要
乳腺癌的生长和扩散的连续阶段依赖于细胞自主因子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信。细胞表面硫酸肝素蛋白多糖Syndecan-1在肿瘤细胞和乳腺肿瘤间质细胞中都是失调的,这表明在这种最常见的女性恶性肿瘤的发病机制中具有潜在的作用。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,影响肿瘤的各种过程,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。本文综述了目前对乳腺癌发生与Syndecan-1表达相关的认识,涉及的机制,并提出了治疗Syndecan-1相关恶性肿瘤的策略。
关键词: 多配体蛋白聚糖,蛋白多糖,乳腺癌,预后,治疗靶点,预后标志物,硫酸乙酰肝素,细胞外基质。
Current Medicinal Chemistry
Title:Syndecan-1 (CD138) as a Pathogenesis Factor and Therapeutic Target in Breast Cancer
Volume: 28 Issue: 25
关键词: 多配体蛋白聚糖,蛋白多糖,乳腺癌,预后,治疗靶点,预后标志物,硫酸乙酰肝素,细胞外基质。
摘要: 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.
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Cite this article as:
Syndecan-1 (CD138) as a Pathogenesis Factor and Therapeutic Target in Breast Cancer, Current Medicinal Chemistry 2021; 28 (25) . https://dx.doi.org/10.2174/0929867328666210629122238
DOI https://dx.doi.org/10.2174/0929867328666210629122238 |
Print ISSN 0929-8673 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-533X |
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