糖和细胞粘附:ST6GalNAc1在前列腺癌进展中的作用

J. Munkley, D. Elliott
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引用次数: 12

摘要

o -链聚糖在癌细胞中发生改变,导致细胞粘附特性的改变并促进转移。但是驱动这些变化的机制以及这些碳水化合物群如何参与肿瘤扩散仍然知之甚少。我们最近发现唾液转移酶基因ST6GalNAc1是前列腺癌中一个新的雄激素调节基因。在小鼠原位移植实验中,前列腺癌细胞中表达ST6GalNAc1可诱导肿瘤相关sTn抗原的表达,降低细胞粘附,显著抑制体内稳定肿瘤块的形成。尽管ST6GalNAc1在原发性前列腺癌组织中显著上调,但在转移性前列腺组织中却显著下调,这表明ST6GalNAc1在前列腺癌进展中起着重要但短暂的作用。在这里,我们讨论了唾液化如何改变前列腺肿瘤细胞的行为和促进癌细胞传播的机制。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Sugars and cell adhesion: the role of ST6GalNAc1 in prostate cancer progression
O-linked glycans become altered in cancer cells, leading to changes in cell adhesive properties and contributing to metastasis. But the mechanisms driving these changes and how these carbohydrate groups are involved in tumour spread remain poorly understood. We recently identified the sialyltransferase gene ST6GalNAc1 as a novel androgen-regulated gene in prostate cancer. Expression of ST6GalNAc1 in prostate cancer cells induced expression of the cancer-associated sTn antigen, reduced cell adhesion, and dramatically inhibited the formation of stable tumour masses in vivo after orthotopic transplantation experiments in mice. Although ST6GalNAc1 is significantly upregulated in primary prostate carcinoma tissue, there is a striking downregulation of this gene in metastatic prostate tissue, suggesting an important yet transient role for ST6GalNAc1 in prostate cancer progression. Here we discuss mechanistically how changes in sialylation could alter prostate tumour cell behaviour and contribute to cancer cell dissemination.
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