Department of Cell, Developmental and Integrative Biology, University of Alabama at Birmingham, Birmingham, AL 35294, USA.
Glycobiology. 2021 Jun 3;31(5):530-539. doi: 10.1093/glycob/cwaa110.
The ST6GAL1 sialyltransferase, which adds α2-6 linked sialic acids to N-glycosylated proteins, is overexpressed in a wide range of human malignancies. Recent studies have established the importance of ST6GAL1 in promoting tumor cell behaviors such as invasion, resistance to cell stress and chemoresistance. Furthermore, ST6GAL1 activity has been implicated in imparting cancer stem cell characteristics. However, despite the burgeoning interest in the role of ST6GAL1 in the phenotypic features of tumor cells, insufficient attention has been paid to the molecular mechanisms responsible for ST6GAL1 upregulation during neoplastic transformation. Evidence suggests that these mechanisms are multifactorial, encompassing genetic, epigenetic, transcriptional and posttranslational regulation. The purpose of this review is to summarize current knowledge regarding the molecular events that drive enriched ST6GAL1 expression in cancer cells.
唾液酸化转移酶 ST6GAL1 将α2-6 连接的唾液酸添加到 N-糖基化蛋白中，在广泛的人类恶性肿瘤中过度表达。最近的研究已经确定了 ST6GAL1 在促进肿瘤细胞行为（如侵袭、抵抗细胞应激和化疗耐药性）中的重要性。此外，ST6GAL1 的活性与赋予癌症干细胞特征有关。然而，尽管人们对 ST6GAL1 在肿瘤细胞表型特征中的作用越来越感兴趣，但对导致肿瘤转化过程中 ST6GAL1 上调的分子机制关注不足。有证据表明，这些机制是多因素的，包括遗传、表观遗传、转录和翻译后调控。本综述的目的是总结目前关于驱动癌细胞中 ST6GAL1 表达丰富的分子事件的知识。
