ArticleClinical & experimental metastasis2009
Cancer cell lines release glutamate into the extracellular environment.
Article in Clinical & experimental metastasis, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers, 1 of them a synthesis that pooled it.
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
51 citing papers in PubMed, 1 synthesis or guideline pooled it, 85 citations in OpenAlex.
- Targeting Ferroptosis as the Achilles' Heel of Breast Cancer: Mechanisms and Therapeutic Opportunities from a Comprehensive Systematic Review.International journal of molecular sciences · 2025Pooled it
- Prediagnostic Plasma Metabolite Profiles and Prediction of Hepatocellular Carcinoma Risk: The Multiethnic Cohort.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2026Article
- Regulation of tumor proliferation by unlocking silent synapses on metastatic cancer cells.bioRxiv : the preprint server for biology · 2026Article
- Peripheral Mechanism of Cancer-Induced Bone Pain.Neuroscience bulletin · 2024Review
- Metabolic collaboration between cells in the tumor microenvironment has a negligible effect on tumor growth.Innovation (Cambridge (Mass.)) · 2024Article
- Colorectal cancer-associated T cell receptor repertoire abnormalities are linked to gut microbiome shifts and somatic cell mutations.Gut microbes · 2023Article
- Review
- Ferroptosis landscape in prostate cancer from molecular and metabolic perspective.Cell death discovery · 2023Review
- Glutamate blunts cell-killing effects of neutrophils in tumor microenvironment.Cancer science · 2022Article
- nNav1.5 expression is associated with glutamate level in breast cancer cells.Biological research · 2022Article
- The Emerging Role of Amino Acids of the Brain Microenvironment in the Process of Metastasis Formation.Cancers · 2021Review
- Article
- SLC1A3 promotes gastric cancer progression via the PI3K/AKT signalling pathway.Journal of cellular and molecular medicine · 2020Article
- Review
- Potential therapeutic treatments of cancer-induced bone pain.Current opinion in supportive and palliative care · 2020Review
- New drugs are not enough‑drug repositioning in oncology: An update.International journal of oncology · 2020Review
- Transient coating of γ-FeBeilstein journal of nanotechnology · 2020Article
- The Evolving Modern Management of Brain Metastasis.Clinical cancer research : an official journal of the American Association for Cancer Research · 2019Review
- Concurrent Targeting of Glutaminolysis and Metabotropic Glutamate Receptor 1 (GRM1) Reduces Glutamate Bioavailability in GRM1Cancer research · 2019Article
- NMDA Receptor Signaling Mediates cFos Expression via Top2β-Induced DSBs in Glioblastoma Cells.Cancers · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Bone is one of the most frequent sites for metastasis of breast and prostate cancers. Bone metastases are associated with pathologic changes in bone turnover and severe pain. The mechanisms that trigger these effects are not well understood, but it is postulated that tumour cells release factors which interfere with signalling processes critical to bone homeostasis. We have identified that several cancer cell lines known to cause bone disruption in animal models of bone metastasis appear to secrete glutamate into their extracellular environment in vitro. Although these cells also express specific glutamate receptors, the implications of this potentially disruptive chemical signal are discussed in relation to normal glutamate-dependent communication processes in bone and a possible mechanistic connection is made between tumour cell glutamate release and the development of pathological changes in bone turnover.
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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.