ST6GAL1 (ST6 Beta-Galactoside Alpha-2,6-Sialyltransferase 1)

By integrating germline (GWAS-based) and somatic evidence, this study provides a comprehensive view of HCC pathogenesis. This integrated strategy successfully identified a core set of genes and proteins with potential causal links to HCC, elucidating their functional convergence in cancer biology. These findings offer novel molecular insights and candidate targets for precise diagnosis, prognostic assessment, and targeted therapy of HCC, laying a solid foundation for future translational research.

Finally, we attempted to illustrate the function of glycosyltransferases and investigate the druggable status of GRGs. Together, our study comprehensively analyzed the causal effect of glycosylation on cancer risk and identified potential strategies for cancer treatment.

These findings demonstrate that ST6GAL1-containing rectal cancer exosomes transfer ST6GAL1 between cells causing treatment resistance.

The expression of glycogenes, such as MGAT1, ST6GAL1, and TUSC3, may be epigenetically regulated. These results suggest that the glycan profile may be at least partly attributable to epigenetic regulation of glycogenes, and that comprehensive glycan profiling could provide clinically useful information for patients with ccRCC.

ST6GAL1 Mediates the Activity of the HIF-HK2 Signalling Pathway in Breast Carcinoma Cells. In our study, in vitro and in vivo models revealed that ST6GAL1 promotes malignant phenotypes in breast cancer cells and regulates the EMT process through activation of the HIF-HK2 signalling pathway.

Finally, we used a recombinant sialic acid cleaving enzyme (sialidase) to confirm that sialoglycans on primary human T cells are bona fide immunophysiological regulators of FasR-driven programmed cell death. Combined, our results demonstrate that sialoglycans on T cells influence cell fate driven by the Fas pathway and provide motivation to further characterize the immunoregulatory roles of the glycocalyx in health and disease.

Finally, we highlight therapeutic strategies that either immunize against PTM neoepitopes or inhibit PTM machinery (e.g., PAD4, OGT, ST6GAL1), with stromal remodeling as an enabling adjunct. PTM biology, spatial omics, and patient sample models can uncover targetable niches and speed up PDAC vaccination, TCR, and enzyme-directed treatment development.

Indeed, a significant reduction in mobility and migration capacity along with increased adhesiveness of GBM cells was observed upon sialyltransferases inhibition. Our findings showed that aberrant expression of different Sias types is crucial for cell migration and adhesion ability of GBM cells, suggesting that Sias might represent biomarkers for GBM and be useful to design innovative therapeutic strategies.

This research is one of the first studies to use ST6GAL1 in preoperative biopsies of patients not scheduled for neoadjuvant treatment. This study revealed highly significant associations of ST6GAL1 expression with HR, HER2, and molecular subtyping. Future studies are recommended to clarify the possible role of ST6GAL1 in resistance to HR and HER2-targeted and other chemotherapeutic agents in BCs.

Our results confirmed that ST6GAL1 decreases the sensitivity of tumor cells to IFNG. This study describes a novel mechanism by which ST6GAL1 promotes the immune escape and malignant progression of CRC.

PD-1 pathway blockade partially restores St6gal1-deficient T cells' ability to control tumor growth. These findings suggest that α2,6-linked sialic acid is critical for maintaining long-term T cell responsiveness, and its loss may contribute to decreased T cell function with age.

The soluble form is absent in the sEVs released from the bone metastatic line C4-2B, which only contains the membrane-bound form. Our results suggest that ST6GAL1 in sEVs derived from PrCa cells may potentially play a role in promoting bone metastasis by facilitating the formation of the pre-metastatic niche.