Gc Sajina, Bellis Susan L, Hjelmeland Anita B
Department of Cell, Developmental and Integrative Biology, University of Alabama at Birmingham, Birmingham, AL, United States.
Front Mol Biosci. 2022 Aug 29;9:962908. doi: 10.3389/fmolb.2022.962908. eCollection 2022.
The Golgi-sialyltransferase ST6Gal1 (βgalactosidase α2,6 sialyltransferase 1), adds the negatively charged sugar, sialic acid, to the terminal galactose of N-glycosylated proteins. Upregulation of ST6Gal1 is observed in many malignancies, and a large body of research has determined that ST6Gal1-mediated α2,6 sialylation impacts cancer hallmarks. ST6Gal1 affects oncogenic behaviors including sustained proliferation, enhanced self-renewal, epithelial-to-mesenchymal transition, invasion, and chemoresistance. However, there are relatively few ST6GaL1 related signaling pathways that are well-established to mediate these biologies: greater delineation of specific targets and signaling mechanisms that are orchestrated by ST6Gal1 is needed. The aim of this review is to provide a summary of our current understanding of select oncogenic signaling pathways and targets affected by ST6Gal1.
高尔基体唾液酸转移酶ST6Gal1（β-半乳糖苷酶α2,6唾液酸转移酶1）将带负电荷的糖——唾液酸添加到N-糖基化蛋白的末端半乳糖上。在许多恶性肿瘤中都观察到ST6Gal1的上调，大量研究已确定ST6Gal1介导的α2,6唾液酸化会影响癌症特征。ST6Gal1影响致癌行为，包括持续增殖、增强自我更新、上皮-间质转化、侵袭和化疗耐药性。然而，相对较少有已明确介导这些生物学过程的ST6Gal1相关信号通路：需要更深入地描绘由ST6Gal1精心编排的特定靶点和信号机制。本综述的目的是总结我们目前对受ST6Gal1影响的特定致癌信号通路和靶点的理解。
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