ArticleThe Journal of biological chemistry2016
Expression of N-Acetylglucosaminyltransferase III Suppresses α2,3-Sialylation, and Its Distinctive Functions in Cell Migration Are Attributed to α2,6-Sialylation Levels.
Article in The Journal of biological chemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
30 citing papers in PubMed, 51 citations in OpenAlex.
- Dynamic Shifts in ER-Plasma Membrane Junctions Signaling Define Pro-Metastatic N-Glycosylation and Predict Prostate Cancer Progression.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Chemoenzymatic Synthesis of Asymmetric Bisecting Bi-, Tri-, and Tetra-AntennaryJournal of the American Chemical Society · 2025Article
- Article
- Specific sialylation of N-glycans and its novel regulatory mechanism.Glycoconjugate journal · 2024Review
- Tolerable glycometabolic stress boosts cancer cell resilience through altered N-glycosylation and Notch signaling activation.Cell death & disease · 2024Article
- Abnormal glycosylation in glioma: related changes in biology, biomarkers and targeted therapy.Biomarker research · 2023Review
- Roles of N-linked glycosylation and glycan-binding proteins in placentation: trophoblast infiltration, immunomodulation, angiogenesis, and pathophysiology.Biochemical Society transactions · 2023Review
- Review
- B4GALT5 high expression associated with poor prognosis of hepatocellular carcinoma.BMC cancer · 2022Article
- Glycomaterials to Investigate the Functional Role of Aberrant Glycosylation in Glioblastoma.Advanced healthcare materials · 2022Review
- Peptide Sequence Mapping around Bisecting GlcNAc-BearingInternational journal of molecular sciences · 2021Article
- Association of ST6GAL1 and CYP19A1 polymorphisms in the 3'-UTR with astrocytoma risk and prognosis in a Chinese Han population.BMC cancer · 2021Article
- Heterogeneity in 2,6-Linked Sialic Acids Potentiates Invasion of Breast Cancer Epithelia.ACS central science · 2021Article
- 3D Structure and Function of Glycosyltransferases Involved inInternational journal of molecular sciences · 2020Review
- ST3Gal IV Mediates the Growth and Proliferation of Cervical Cancer CellsFrontiers in oncology · 2020Article
- Bisecting GlcNAc Is a General Suppressor of Terminal Modification ofMolecular & cellular proteomics : MCP · 2019Article
- N-Glycosylation in progression of skin cancer.Medical oncology (Northwood, London, England) · 2019Review
- Aberrant glycosylation and cancer biomarker discovery: a promising and thorny journey.Clinical chemistry and laboratory medicine · 2019Review
- N-Glycomic and Transcriptomic Changes Associated with CDX1 mRNA Expression in Colorectal Cancer Cell Lines.Cells · 2019Article
- A complex between phosphatidylinositol 4-kinase IIα and integrin α3β1 is required forThe Journal of biological chemistry · 2019Article
Corrections and comments
- Commented on by
Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
N-Acetylglucosaminyltransferase III (GnT-III), which catalyzes the addition of the bisecting GlcNAc branch on N-glycans, is usually described as a metastasis suppressor. Overexpression of GnT-III inhibited migration in multiple types of tumor cells. However, these results seem controversial to the clinical observations for the increased expression of GnT-III in human hepatomas, glioma, and ovarian cancers. Here, we present evidence that these inconsistencies are mainly attributed to the different expression pattern of cell sialylation. In detail, we show that overexpression of GnT-III significantly inhibits α2,3-sialylation but not α2,6-sialylation. The migratory ability of cells without or with a low level of α2,6-sialylation is consistently suppressed after GnT-III overexpression. In contrast, the effects of GnT-III overexpression are variable in tumor cells that are highly α2,6-sialylated. Overexpression of GnT-III promotes the cell migration in glioma cells U-251 and hepatoma cells HepG2, although it has little influence in human breast cancer cell MDA-MB-231 and gastric cancer cell MKN-45. Interestingly, up-regulation of α2,6-sialylation by overexpressing β-galactoside α2,6-sialyltranferase 1 in the α2,6-hyposialylated HeLa-S3 cells abolishes the anti-migratory effects of GnT-III. Conversely, depletion of α2,6-sialylation by knock-out of β-galactoside α2,6-sialyltranferase 1 in α2,6-hypersialylated HepG2 cells endows GnT-III with the anti-migratory ability. Taken together, our data clearly demonstrate that high expression of α2,6-sialylation on the cell surface could affect the anti-migratory role of GnT-III, which provides an insight into the mechanistic roles of GnT-III in tumor metastasis.
Indexed as
Identifiers
What OpenQuestion holds
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.