ArticleLeukemia2025
The glycosyltransferase ST3GAL4 drives immune evasion in acute myeloid leukemia by synthesizing ligands for the glyco-immune checkpoint receptor Siglec-9.
Article in Leukemia, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed.
- Sialic acidOncoimmunology · 2026Article
- From Glycocode to Precision Oncology: Therapeutic Strategies Targeting Aberrant O-GalNAc Glycosylation in Cancer.Chemical reviews · 2026Review
- Rapid discovery of cell-surface glycosylation regulators using a lectin-based magnetic CRISPR screen.Cell reports methods · 2026Article
- Immune implications and therapeutic opportunities of tumor glycosylation.Nature cancer · 2026Review
- Upregulation of GnT-IVa and Its Critical Roles in ATRA-Induced Differentiation of Acute Promyelocytic Leukemia Cells.Biomolecules · 2026Article
- Glucose metabolic reprogramming as a driver of immunosuppression in the tumour microenvironment.Clinical and translational medicine · 2026Review
- Aberrant glycosylation in hematologic malignancies: mechanisms, immune evasion, and therapeutic targeting.Blood cancer journal · 2026Review
- CRISPR activation screens map the genomic landscape of cancer glycome remodeling.Cell genomics · 2026Article
- Revealing cancer glycome drivers using CRISPR activation screens.Cell genomics · 2026Article
- Systematic Pan-Cancer Characterization of ST3GAL4 Reveals Its Prognostic and Immunologic Associations.Biomedicines · 2026Article
- Writers and readers of sialylation in immunoregulation in cancer.The Journal of biological chemistry · 2026Review
- Homoharringtonine Promotes FTO Degradation to Suppress LILRB4-Mediated Immune Evasion in Acute Monocytic Leukaemia.Cell proliferation · 2026Article
- Specific Recognition of Glycoproteins: Design Strategies and Application Prospects of Molecularly Imprinted Polymers.International journal of molecular sciences · 2026Review
- Immune-tumor cell ligand-receptor axes driving metabolic reprogramming and therapeutic resistance in cancer.Frontiers in immunology · 2026Review
- Sialylation in Thyroid Carcinoma: An Overview of Mechanisms, Markers, and Therapeutic Opportunities.Journal of Cancer · 2026Review
- Transmembrane lectins in cancer immunity: emerging drivers of myeloid-mediated immunosuppression.Frontiers in immunology · 2026Review
- Multi-omics analysis of ST3GAL4-mediated lacto/neolacto glycosphingolipid metabolism reveals immune evasion and poor prognosis in TNBC.Frontiers in immunology · 2026Article
- Plasma metabolic landscape unveils key regulators of leukemia subtype progression.Future science OA · 2025Article
- Review
- Polysialic acid is upregulated on activated immune cells and negatively regulates anticancer immune activity.Frontiers in oncology · 2025Article
Corrections and comments
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Authors and funding
11 authors.
Funding
Abstract
Immunotherapy has demonstrated promise as a treatment for acute myeloid leukemia (AML). However, there is still an urgent need to identify new molecules that inhibit the immune response to AML. Most prior research in this area has focused on protein-protein interaction interfaces. While carbohydrates also regulate immune recognition, the role of cell-surface glycans in driving AML immune evasion is comparatively understudied. The Siglecs, for example, are an important family of inhibitory, glycan-binding signaling receptors that have emerged as prime targets for cancer immunotherapy in recent years. In this study, we find that AML cells express ligands for the receptor Siglec-9 at high levels. Integrated CRISPR genomic screening and clinical bioinformatic analysis identified ST3GAL4 as a potential driver of Siglec-9 ligand expression in AML. Depletion of ST3GAL4 by CRISPR-Cas9 knockout (KO) dramatically reduced the expression of Siglec-9 ligands in AML cells. Mass spectrometry analysis of cell-surface glycosylation in ST3GAL4 KO cells revealed that Siglec-9 primarily binds N-linked sialoglycans on these cell types. Finally, we found that ST3GAL4 KO enhanced the sensitivity of AML cells to phagocytosis by Siglec-9-expressing macrophages. This work reveals a novel axis of immune evasion and implicates ST3GAL4 as a possible target for immunotherapy in AML.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.