B3GNT5 (beta-1,3-N-acetylglucosaminyltransferase 5) is a glycosyltransferase involved in synthesizing lactoseries glycosphingolipids (GSLs), which mediate cell adhesion, immune regulation, and cancer stemness . The B3GNT5 antibody is a purified immunoglobulin developed to detect and inhibit this enzyme, enabling researchers to study its biological and pathological roles .
The B3GNT5 antibody has been pivotal in elucidating the enzyme’s role in tumorigenesis:
Immune Regulation: Antibody-driven inhibition of B3GNT5 reduces T cell-mediated anti-tumor responses by suppressing cytokine communication and CD8+ T cell activation .
Cancer Stemness: In pancreatic adenocarcinoma (PAAD), B3GNT5 knockdown via antibody-mediated targeting diminishes sphere-forming ability and self-renewal capacity of cancer stem cells (CSCs) .
Tumor Microenvironment (TME): B3GNT5 expression correlates with stromal/immune cell infiltration scores and epithelial-mesenchymal transition (EMT) in cancers like glioblastoma (GBM) and lung adenocarcinoma (LUAD) .
Pathway Modulation: B3GNT5 regulates DNA repair, oxidative phosphorylation, and KRAS signaling pathways, as shown by gene set enrichment analysis (GSEA) .
Glycosphingolipid Synthesis: The antibody confirms reduced lactoseries GSL levels in B3GNT5-deficient cells, impacting cell-cell adhesion in pre-implantation embryos .
A pan-cancer analysis of 33 tumor types revealed the following :
| Cancer Type | Role of B3GNT5 | Antibody Application |
|---|---|---|
| Pancreatic Adenocarcinoma | Drives tumor progression, stemness, and chemotherapy resistance | Sphere-formation assays, Western blot validation |
| Lung Adenocarcinoma | Correlates with immune checkpoint expression (PD-L1, CTLA-4) | Immune infiltration scoring |
| Breast Cancer | Linked to cytokine communication and poor prognosis | GSEA for pathway enrichment |
| Glioblastoma | Associated with stromal activation and reduced tumor purity | ESTIMATE algorithm for TME analysis |
Prognostic Marker: High B3GNT5 expression predicts poor survival in PAAD, LUAD, and BRCA .
Therapeutic Target: Antibody-mediated B3GNT5 inhibition suppresses CSC stemness and enhances chemosensitivity in pancreatic cancer models .
Immune Evasion: B3GNT5 promotes TGF-β/CCL2 secretion by CSCs, recruiting regulatory T cells (Tregs) and macrophages to dampen anti-tumor immunity .
While the B3GNT5 antibody has advanced mechanistic studies, further work is needed to: