ArticleOncology reports2020
ACSL4 suppresses glioma cells proliferation via activating ferroptosis.
Article in Oncology reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 132 papers, 2 of them syntheses 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
132 citing papers in PubMed, 2 syntheses or guidelines pooled it, 188 citations in OpenAlex.
- Global research status, hotspots and prospects of ferroptosis in glioma: a scientometric analysis.Frontiers in cellular neuroscience · 2025Pooled it
- A Systematic Review of Nanoparticle-Mediated Ferroptosis in Glioma Therapy.International journal of nanomedicine · 2025Pooled it
- Molecular mechanisms of iron metabolism and ferroptosis in cardiovascular diseases and intervention strategies targeting natural products (Review).Molecular medicine reports · 2026Review
- Wogonin Suppresses Non-Small Cell Lung Cancer Growth in Association with Oxidative Stress, c-Myc/GPX4 Downregulation and Ferroptosis-Related Responses.Antioxidants (Basel, Switzerland) · 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
- From Integrated Analysis to Clinical Insight: ncRNA-Mediated Ferroptosis in Glioblastoma.Cancers · 2026Review
- DDX3 inhibits PTZ-induced ferroptosis in human neuronal SH-SY5Y cells via Wnt/β-catenin signaling.In vitro cellular & developmental biology. Animal · 2026Article
- Comprehensive analysis of the potential role of Ferroptosis-related genes in glioblastoma multiforme.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2026Article
- Ferroptosis and metabolic reprogramming in the immunosuppressive microenvironment of glioblastoma: emerging mechanisms and novel strategies.Frontiers in immunology · 2026Review
- Targeting Programmed Cell Death in Depression: A Review of Traditional Chinese Medicine Interventions Based on Preclinical Evidence.Neuropsychiatric disease and treatment · 2026Review
- Metabolic remodeling and immune evasion in glioblastoma: a focus on serine and lipid networks.Frontiers in oncology · 2026Review
- From scavenger to victim: mechanism and treatment of microglial ferroptosis in white matter injury disease.Frontiers in immunology · 2026Review
- Exploring the diagnostic and prognostic potential of LCFAs' metabolic and biosynthetic pathways in glioblastoma multiforme using a bioinformatics approach.Research in pharmaceutical sciences · 2025Article
- Long-chain acyl-CoA synthetases: biological functions, diseases and therapeutic targets.Molecular biomedicine · 2025Review
- ACSL6 modulates docosahexaenoic acid-induced cytotoxicity to potentiate chemotherapy response in colorectal and breast cancer.Oncogenesis · 2025Article
- Proanthocyanidin and mitoglitazone suppress lipogenesis by targeting ferroptosis in metabolic dysfunction-associated steatohepatitis.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Oxidative Stress and Antioxidants in Glioblastoma: Mechanisms of Action, Therapeutic Effects and Future Directions.Antioxidants (Basel, Switzerland) · 2025Review
- Ferroptosis as a therapeutic target in glioblastoma: Mechanisms and emerging strategies.Molecular therapy. Nucleic acids · 2025Review
- Ioning out glioblastoma: ferroptosis mechanisms and therapeutic frontiers.Cell death discovery · 2025Review
72 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
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acyl‑CoA synthetase long‑chain family member 4 (ACSL4) is a member of the long chain family of acyl‑CoA synthetase proteins, which have recently been shown to serve an important role in ferroptosis. Previous studies have suggested that ferroptosis is involved in the occurrence of glioma; however, the role of ACSL4 in glioma remains unknown. In the present study, a reduction of ferroptosis in human glioma tissues and glioma cells was observed. Subsequently, it was demonstrated that the expression of ACSL4 was also downregulated in human glioma tissues and cells. A ferroptosis inhibitor and inducer were used to investigate the effects of ferroptosis on viability. The results showed that promoting ferroptosis inhibited the proliferation of glioma cells, and that the use of inducers had the reverse effect. Therefore, it was hypothesized that the reduction in ACSL4 expression may have been involved in ferroptosis and proliferation in glioma. Overexpression of ACSL4 decreased expression of glutathione peroxidase 4 and increased the levels of ferroptotic markers, including 5‑hydroxyeicosatetraenoic (HETE), 12‑HETE and 15‑HETE. Additionally, ACSL4 overexpression resulted in an increase in lactate dehydrogenase release and a reduction in cell viability. The opposite results were observed when ACSL4 was silenced. These findings suggest that ACSL4 regulates ferroptosis and proliferation of glioma cells. To further investigate the mechanism underlying ACSL4‑mediated regulation of proliferation in glioma cells, cells were treated with small interfering (si)‑ACSL4 and sorafenib, a ferroptosis inducer. sorafenib attenuated the ability of siRNA‑mediated silencing of ACSL4, thus improving cell viability. These results demonstrate that ACSL4 protects glioma cells and exerts anti‑proliferative effects by activating a ferroptosis pathway and highlight the pivotal role of ferroptosis regulation by ACSL4 in its protective effects on glioma. Therefore, ACSL4 may serve as a novel therapeutic target for the treatment of glioma.
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.