ArticleMolecular and cellular biology2003
Polysialic acid directs tumor cell growth by controlling heterophilic neural cell adhesion molecule interactions.
Article in Molecular and cellular biology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.
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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.
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Who cites it
58 citing papers in PubMed, 190 citations in OpenAlex.
- Aberrant sialic acid metabolism promotes metabolic reprogramming and metastasis in breast cancer.Frontiers in oncology · 2025Article
- Glycosylation in Cancer.Handbook of experimental pharmacology · 2025Review
- The Bifunctional Effects of Lactoferrin (LFcinB11) in Inhibiting Neural Cell Adhesive Molecule (NCAM) Polysialylation and the Release of Neutrophil Extracellular Traps (NETs).International journal of molecular sciences · 2024Article
- When a negative (charge) is not a positive: sialylation and its role in cancer mechanics and progression.Frontiers in oncology · 2024Review
- Fucosyltransferase 3 and 8 promote the metastatic capacity of cancer stem-like cells via CD15s and E-cadherin in esophageal cancer.Iranian journal of basic medical sciences · 2024Article
- Glycocalyx transduces membrane leak in brain tumor cells exposed to sharp magnetic pulsing.Biophysical journal · 2023Article
- Proinflammatory Macrophage Activation by the Polysialic Acid-Siglec-16 Axis Is Linked to Increased Survival of Patients with Glioblastoma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2023Article
- The Graphical Studies of the Major Molecular Interactions for Neural Cell Adhesion Molecule (NCAM) Polysialylation by Incorporating Wenxiang Diagram into NMR Spectroscopy.International journal of molecular sciences · 2022Article
- Functional Diversity of Neuronal Cell Adhesion and Recognition Molecule L1CAM through Proteolytic Cleavage.Cells · 2022Review
- Review
- EPIMUTESTR: a nearest neighbor machine learning approach to predict cancer driver genes from the evolutionary action of coding variants.Nucleic acids research · 2022Article
- Recent advances on smart glycoconjugate vaccines in infections and cancer.The FEBS journal · 2022Review
- News and Views on Polysialic Acid: From Tumor Progression and Brain Development to Psychiatric Disorders, Neurodegeneration, Myelin Repair and Immunomodulation.Frontiers in cell and developmental biology · 2022Review
- Cell Adhesion Molecules in Neuroblastoma: Complex Roles, Therapeutic Potential.Frontiers in oncology · 2022Review
- Review
- Neural cell adhesion molecule is required for ventricular conduction system development.Development (Cambridge, England) · 2021Article
- EndoN treatment allows neuroblasts to leave the rostral migratory stream and migrate towards a lesion within the prefrontal cortex of rats.Neural regeneration research · 2020Article
- Sialic Acid Metabolic Engineering of Breast Cancer Cells Interferes with Adhesion and Migration.Molecules (Basel, Switzerland) · 2020Article
- Pulsed Low-Frequency Magnetic Fields Induce Tumor Membrane Disruption and Altered Cell Viability.Biophysical journal · 2020Article
- Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Polysialic acid (PSA), a carbohydrate polymer attached to the neural cell adhesion molecule (NCAM), promotes neural plasticity and tumor malignancy, but its mode of action is controversial. Here we establish that PSA controls tumor cell growth and differentiation by interfering with NCAM signaling at cell-cell contacts. Interactions between cells with different PSA and NCAM expression profiles were initiated by enzymatic removal of PSA and by ectopic expression of NCAM or PSA-NCAM. Removal of PSA from the cell surface led to reduced proliferation and activated extracellular signal-regulated kinase (ERK), inducing enhanced survival and neuronal differentiation of neuroblastoma cells. Blocking with an NCAM-specific peptide prevented these effects. Combinatorial transinteraction studies with cells and membranes with different PSA and NCAM phenotypes revealed that heterophilic NCAM binding mimics the cellular responses to PSA removal. In conclusion, our data demonstrate that PSA masks heterophilic NCAM signals, having a direct impact on tumor cell growth. This provides a mechanism for how PSA may promote the genesis and progression of highly aggressive PSA-NCAM-positive tumors.
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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.