ArticleProceedings of the National Academy of Sciences of the United States of America2016
Glycolipid GD3 and GD3 synthase are key drivers for glioblastoma stem cells and tumorigenicity.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers.
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Who cites it
70 citing papers in PubMed, 103 citations in OpenAlex.
- Review
- Ganglioside therapy in cancer molecular insights and therapeutic opportunities.Discover oncology · 2025Review
- Glioblastoma: A Multidisciplinary Approach to Its Pathophysiology, Treatment, and Innovative Therapeutic Strategies.Biomedicines · 2025Review
- The GD3 ganglioside promotes cell growth, plasticity and chemotherapy resistance of human glioblastoma cancer stem cells.Cancer cell international · 2025Article
- GD2 is a Crucial Ganglioside in the Signal Modulation and Application as a Target of Cancer Therapeutics.Cancer science · 2025Review
- Ganglioside GD2 Contributes to a Stem-Like Phenotype in Intrahepatic Cholangiocarcinoma.Liver international : official journal of the International Association for the Study of the Liver · 2025Article
- Action Mechanisms of Exosomes Derived from GD3/GD2-Positive Glioma Cells in the Regulation of Phenotypes and Intracellular Signaling: Roles of Integrins.International journal of molecular sciences · 2024Article
- Emerging role of MAPK signaling in glycosphingolipid-associated tumorigenesis.Glycoconjugate journal · 2024Review
- Crucial roles of exosomes secreted from ganglioside GD3/GD2-positive glioma cells in enhancement of the malignant phenotypes and signals of GD3/GD2-negative glioma cells.Nagoya journal of medical science · 2024Article
- Glioma-Associated Sialoglycans Drive the Immune Suppressive Phenotype and Function of Myeloid Cells.Pharmaceutics · 2024Article
- GD2 and its biosynthetic enzyme GD3 synthase promote tumorigenesis in prostate cancer by regulating cancer stem cell behavior.Scientific reports · 2024Article
- Hu14.18K.322A Causes Direct Cell Cytotoxicity and Synergizes with Induction Chemotherapy in High-Risk Neuroblastoma.Cancers · 2024Article
- Advances in Mass Spectrometry of Gangliosides Expressed in Brain Cancers.International journal of molecular sciences · 2024Review
- A modular chemoenzymatic cascade strategy for the structure-customized assembly of ganglioside analogs.Communications chemistry · 2024Article
- The good, the bad, and the unknown nature of decreased GD3 synthase expression.Frontiers in molecular neuroscience · 2024Article
- When a negative (charge) is not a positive: sialylation and its role in cancer mechanics and progression.Frontiers in oncology · 2024Review
- The Ying and Yang of Ganglioside Function in Cancer.Cancers · 2023Review
- Deciphering the Action of Neuraminidase in Glioblastoma Models.International journal of molecular sciences · 2023Article
- Review
- Possible regulation of ganglioside GD3 synthase gene expression with DNA methylation in human glioma cells.Glycoconjugate journal · 2023Article
10 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The cancer stem cells (CSCs) of glioblastoma multiforme (GBM), a grade IV astrocytoma, have been enriched by the expressed marker CD133. However, recent studies have shown that CD133(-) cells also possess tumor-initiating potential. By analysis of gangliosides on various cells, we show that ganglioside D3 (GD3) is overexpressed on eight neurospheres and tumor cells; in combination with CD133, the sorted cells exhibit a higher expression of stemness genes and self-renewal potential; and as few as six cells will form neurospheres and 20-30 cells will grow tumor in mice. Furthermore, GD3 synthase (GD3S) is increased in neurospheres and human GBM tissues, but not in normal brain tissues, and suppression of GD3S results in decreased GBM stem cell (GSC)-associated properties. In addition, a GD3 antibody is shown to induce complement-dependent cytotoxicity against cells expressing GD3 and inhibition of GBM tumor growth in vivo. Our results demonstrate that GD3 and GD3S are highly expressed in GSCs, play a key role in glioblastoma tumorigenicity, and are potential therapeutic targets against GBM.
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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.