细胞表面受体在细胞对细胞外配体的反应中发挥着至关重要的作用，有助于根据来自细胞外的信息调节细胞的功能。 Syndecan 是指调节细胞外和胞质事件的细胞粘附受体家族。多聚糖表达的改变会以细胞类型特异性的方式破坏调节机制，通常导致严重的疾病，尤其是癌症。鉴于多配体聚糖的多方面功能和独特的组织分布，阐明多配体聚糖表达的基因水平复杂性，从而进一步了解其在各种致癌过程中的参与非常重要。尽管越来越多的证据表明多聚糖家族成员的蛋白质表达模式在癌细胞中显着改变，但潜在的基因水平机制仍然很大程度上未知。本综述致力于通过利用 cBioPortal 等工具仔细检查广泛的癌症基因组数据集，探索不同癌症类型的多配体基因表达水平。我们的分析表明，SDC 基因的体细胞突变很少发生，而拷贝数改变在多种癌症中经常观察到，特别是在 SDC2 和 SDC4 中。值得注意的是，SDC2 和 SDC4 的扩增与转移潜能增加和预后不良相关。这强调了 SDC2 和 SDC4 扩增在致癌过程中反复出现的性质，并揭示了它们通过增强蛋白质表达促进癌症活动的作用。这些扩增的鉴定不仅丰富了我们对致癌机制的理解，而且还暗示了靶向SDC2和SDC4以抑制癌细胞增殖和转移的潜在治疗途径。

Cell surface receptors play crucial roles in cellular responses to extracellular ligands, helping to modulate the functions of a cell based on information coming from outside the cell. Syndecan refers to a family of cell adhesion receptors that regulate both extracellular and cytosolic events. Alteration of syndecan expression disrupts regulatory mechanisms in a cell type-specific fashion, often leading to serious diseases, notably cancer. Given the multifaceted functions and distinct tissue distributions of syndecan, it will be important to unravel the gene-level intricacies of syndecan expression and thereby further understand its involvement in various carcinogenic processes. Although accumulating evidence indicates that the protein expression patterns of syndecan family members are significantly altered in cancer cells, the underlying gene-level mechanisms remain largely unknown. This review endeavors to explore syndecan gene expression levels across different cancer types by scrutinizing extensive cancer genome datasets utilizing tools such as cBioPortal. Our analysis unveils that somatic mutations in SDC genes are rare occurrences, whereas copy number alterations are frequently observed across diverse cancers, particularly in SDC2 and SDC4. Notably, amplifications of SDC2 and SDC4 correlate with heightened metastatic potential and dismal prognosis. This underscores the recurrent nature of SDC2 and SDC4 amplifications during carcinogenesis and sheds light on their role in promoting cancer activity through augmented protein expression. The identification of these amplifications not only enriches our understanding of carcinogenic mechanisms but also hints at the potential therapeutic avenue of targeting SDC2 and SDC4 to curb cancer cell proliferation and metastasis.