ArticleCancer research2009
GD3, an overexpressed tumor-derived ganglioside, mediates the apoptosis of activated but not resting T cells.
Article in Cancer research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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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.
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Who cites it
41 citing papers in PubMed, 60 citations in OpenAlex.
- Nifetepimine, a dihydropyrimidone, ensures CD4+ T cell survival in a tumor microenvironment by maneuvering sarco(endo)plasmic reticulum Ca2+ ATPase (SERCA).The Journal of biological chemistry · 2012Trial
- Ganglioside GD2 identifies breast cancer stem cells and promotes tumorigenesis.The Journal of clinical investigation · 2012Trial
- Gangliosides GM3 And GD3 Modulate Insulin Aggregation Pathways and Reduce Cytotoxicity Through Structural Remodeling.bioRxiv : the preprint server for biology · 2026Article
- EDF1 accelerates ganglioside GD3 accumulation to boost CD52-mediated CD8Journal of experimental & clinical cancer research : CR · 2025Article
- Current state-of-the-art on ganglioside-mediated immune modulation in the tumor microenvironment.Cancer metastasis reviews · 2023Review
- Apoptosis: aJournal for immunotherapy of cancer · 2023Review
- The biological role and immunotherapy of gangliosides and GD3 synthase in cancers.Frontiers in cell and developmental biology · 2023Review
- The Molecular and Cellular Strategies of Glioblastoma and Non-Small-Cell Lung Cancer Cells Conferring Radioresistance.International journal of molecular sciences · 2022Review
- Structure and function of glycosphingolipids on small extracellular vesicles.Glycoconjugate journal · 2022Review
- Sialic acid O-acetylation: From biosynthesis to roles in health and disease.The Journal of biological chemistry · 2021Review
- The Role of NKT Cells in Glioblastoma.Cells · 2021Review
- An Immunosuppressive Effect of Melanoma-derived Exosomes on NY-ESO-1 Antigen-specific Human CD8Immunological investigations · 2020Article
- The roles of curcumin in regulating the tumor immunosuppressive microenvironment.Oncology letters · 2020Review
- Profiling ofInternational journal of molecular sciences · 2020Article
- Effects of Gangliosides on Spermatozoa, Oocytes, and Preimplantation Embryos.International journal of molecular sciences · 2019Review
- Gangliosides: The Double-Edge Sword of Neuro-Ectodermal Derived Tumors.Biomolecules · 2019Review
- Sialic Acid-Dependent Inhibition of T Cells by Exosomal Ganglioside GD3 in Ovarian Tumor Microenvironments.Journal of immunology (Baltimore, Md. : 1950) · 2018Article
- Ganglioside GD3 synthase (GD3S), a novel cancer drug target.Acta pharmaceutica Sinica. B · 2018Review
- Expression of ganglioside GD2, reprogram the lipid metabolism and EMT phenotype in bladder cancer.Oncotarget · 2017Article
- Reprogramming the tumor microenvironment: tumor-induced immunosuppressive factors paralyze T cells.Oncoimmunology · 2015Review
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
We previously elucidated an important role for gangliosides in renal cell carcinoma-mediated T lymphocyte apoptosis, although the mechanism by which they mediated lymphocyte death remained unclear. Here, we show that when added in purified form, GD3 is internalized by activated T cells, initiating a series of proapoptotic events, including the induction of reactive oxygen species (ROS), an enhancement of p53 and Bax accumulation, an increase in mitochondrial permeability, cytochrome c release, and the activation of caspase-9. GD3-induced apoptosis of activated T cells was dose dependent and inhibitable by pretreating the lymphocytes with N-acetylcysteine, cyclosporin A, or bongkrekic acid, emphasizing the essential role of ROS and mitochondrial permeability to the process. Ganglioside-induced T-cell killing was associated with the caspase-dependent degradation of nuclear factor-kappaB-inducible, antiapoptotic proteins, including RelA; this suggests that their loss is initiated only after the cascade is activated and that their disappearance amplifies but not triggers GD3 susceptibility. Resting T cells did not internalize appreciable levels of GD3 and did not undergo any of the proapoptotic changes that characterize activated T lymphocytes exposed to the ganglioside. RelA overexpression endows Jurkat cells with resistance to GD3-mediated apoptosis, verifying the role of the intact transcription factor in mediating protection from the ganglioside.
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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.