ArticleOncotarget2016
Sulfasalazine impacts on ferroptotic cell death and alleviates the tumor microenvironment and glioma-induced brain edema.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 88 papers, 2 of them syntheses that pooled it.
What it found
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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.
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
88 citing papers in PubMed, 2 syntheses or guidelines pooled it, 125 citations in OpenAlex.
- Pharmacological targeting of xCT/system Xc- to modulate temozolomide sensitivity in glioma and glioblastoma preclinical models: a focused systematic review.Cancer chemotherapy and pharmacology · 2026Pooled it
- Ferroptosis in glioma treatment: Current situation, prospects and drug applications.Frontiers in oncology · 2022Pooled it
- Pharmacological targeting of ferroptosis in cancer: mechanisms, tumor immunity, and translational challenges.Pharmacological reports : PR · 2026Review
- Repurposing approved drugs as ferroptosis modulators: a critical review of clinical trials in cancer and neurodegeneration.Naunyn-Schmiedeberg's archives of pharmacology · 2026Review
- Targeting Ferroptosis in Glioblastoma: Molecular Mechanisms, Tumor Microenvironment, and Therapeutic Opportunities.Cancers · 2026Review
- Targeting programmed cell death: a novel therapeutic paradigm for cancer based on mode-of-death classification.Apoptosis : an international journal on programmed cell death · 2026Review
- Ferroptosis in Neuropsychiatric and Neurodegenerative Disorders: Shared Mechanisms and Disease-Specific Signatures.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Time-Resolved Transcriptomic Profiling of Chandipura Virus Infection Reveals Dynamic Host Responses and Host-Directed Therapeutic Targets.International journal of molecular sciences · 2026Article
- ATM functions as a rheostat of metabolic stress in small-cell lung cancer.bioRxiv : the preprint server for biology · 2026Article
- Advances in ferroptosis for castration-resistant prostate cancer treatment: novel drug targets and combination therapy strategies.Prostate cancer and prostatic diseases · 2026Review
- Beyond synapses non-synaptic neural microenvironment interactions remodel circuits and drive glioma progression.Frontiers in oncology · 2026Review
- Progress in research on the mechanisms and therapeutic strategies of SLC7A11 regulation in glioma.Discover oncology · 2025Review
- Ferroptosis, autophagy, and mitochondrial dynamics: Front burners in cancer therapeutics.World journal of clinical oncology · 2025Article
- Emerging Roles of Ferroptosis in Skin Pathophysiology.The Journal of investigative dermatology · 2025Review
- Ferroptosis as a therapeutic target in glioblastoma: Mechanisms and emerging strategies.Molecular therapy. Nucleic acids · 2025Review
- Role of Glutamate Excitotoxicity in Glioblastoma Growth and Its Implications in Treatment.Cell biology international · 2025Review
- SIRT5-mediated BCAT1 desuccinylation and stabilization leads to ferroptosis insensitivity and promotes cell proliferation in glioma.Cell death & disease · 2025Article
- Breaking Down Glioma-Microenvironment Crosstalk.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2025Review
- Advances in understanding ferroptosis mechanisms and their impact on immune cell regulation and tumour immunotherapy.Discover oncology · 2025Review
- Nanoparticle-Mediated Ferroptosis for Cancer Therapy: Mechanisms and Therapeutic Strategies.Nanotechnology, science and applications · 2025Review
28 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The glutamate transporter xCT (SCL7a11, system Xc-, SXC) is an emerging key player in glutamate/cysteine/glutathione homeostasis in the brain and in cancer. xCT expression correlates with the grade of malignancy. Here, we report on the use of the U.S. Food and Drug Administration and EMA-approved xCT inhibitor, sulfasalazine (SAS) in gliomas. SAS does not affect cell viability in gliomas at concentrations below 200 µM. At higher concentrations SAS becomes gliomatoxic. Mechanistically SAS inhibits xCT and induces ferroptotic cell death in glioma cells. There is no evidence for impact on autophagic flux following SAS application. However, SAS can potentiate the efficacy of the standard chemotherapeutic and autophagy-inducing agent temozolomide (Temcat, Temodal or Temodar®). We also investigated SAS in non-transformed cellular constituents of the brain. Neurons and brain tissue are almost non-responding to SAS whereas isolated astrocytes are less sensitive towards SAS toxicity compared to gliomas. In vivo SAS treatment does not affect experimental tumor growth and treated animals revealed comparable tumor volume as untreated controls. However, SAS treatment resulted in reduced glioma-derived edema and, hence, total tumor volume burden as revealed by T2-weighted magnetic resonance imaging. Altogether, we show that SAS can be utilized for targeting the glutamate antiporter xCT activity as a tumor microenvironment-normalizing drug, while crucial cytotoxic effects in brain tumors are minor.
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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.