ReviewDiscover oncology2025
Progress in research on the mechanisms and therapeutic strategies of SLC7A11 regulation in glioma.
Review in Discover oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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
3 citing papers in PubMed.
- miR-15a-5p Regulates Ferroptosis in Glioblastoma by Targeting GLS2.CNS neuroscience & therapeutics · 2026Article
- Molecular Effects of Indocyanine Green-Photodynamic Therapy on Programmed Cell Death Pathways in T98G and U-118MG Glioblastoma Cells-An RT-qPCR Study.Current issues in molecular biology · 2026Article
- Targeting Ferroptosis in Glioblastoma: Molecular Mechanisms, Tumor Microenvironment, and Therapeutic Opportunities.Cancers · 2026Review
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.
Funding
Abstract
This review summarizes the critical role of SLC7A11 in the pathogenesis of glioma and its potential as a therapeutic target. By mediating cystine uptake and glutamate release, SLC7A11 promotes glutathione (GSH) synthesis, protecting glioma cells from oxidative stress-induced damage and maintaining the antioxidant defense mechanisms. Its expression levels are closely correlated with glioma malignancy and prognosis, with significantly elevated expression observed in high-grade gliomas, suggesting its involvement in malignant progression. Therapeutically, high SLC7A11 expression is associated with resistance to radiotherapy and chemotherapy, making it an attractive target. Studies have shown that inhibiting SLC7A11 function (e.g., using sulfasalazine) reduces GSH synthesis, induces reactive oxygen species (ROS) accumulation, and triggers ferroptosis in glioma cells. Furthermore, molecules such as p53, p62, and OTUB1 regulate SLC7A11 expression, influencing glioma development. Therapeutic strategies targeting SLC7A11, including the application of inhibitors and exploration of molecular targets, offer novel directions for glioma treatment.
Indexed as
Identifiers
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.