ArticleOncotarget2017
Identification of aurintricarboxylic acid as a selective inhibitor of the TWEAK-Fn14 signaling pathway in glioblastoma cells.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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.
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Who cites it
29 citing papers in PubMed, 50 citations in OpenAlex.
- Research progress on TWEAK/Fn14 signaling in chronic wound healing.Frontiers in surgery · 2026Review
- Aurintricarboxylic Acid Attenuates Tramadol Withdrawal Syndrome Via TWEAK/FN14 Inhibition and CREB Modulation in Mice Model.Neuromolecular medicine · 2025Article
- Proposed Hypothesis of TWEAK/Fn14 Receptor Modulation in Autism Spectrum Disorder.CNS & neurological disorders drug targets · 2025Review
- Aurintricarboxylic acid inhibits the malignant phenotypes of drug-resistant cells via translation regulation.Frontiers in oncology · 2025Article
- The CD163/TWEAK/Fn14 axis: A potential therapeutic target for alleviating inflammatory bone loss.Journal of orthopaedic translation · 2024Article
- Magnesium enhances aurintricarboxylic acid's inhibitory action on the plasma membrane CaScientific reports · 2024Article
- TWEAK Signaling-Induced ID1 Expression Drives Malignant Transformation of Hepatic Progenitor Cells During Hepatocarcinogenesis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- Inhibition of TWEAK/Tnfrsf12a axis protects against acute liver failure by suppressing RIPK1-dependent apoptosis.Cell death discovery · 2022Article
- Inhibitors of DNA Methylation.Advances in experimental medicine and biology · 2022Review
- Aurintricarboxylic acid is a canonical disruptor of the TAZ-TEAD transcriptional complex.PloS one · 2022Article
- Quinacrine-CASIN combination overcomes chemoresistance in human acute lymphoid leukemia.Nature communications · 2021Article
- Lysosomal Function Impacts the Skeletal Muscle Extracellular Matrix.Journal of developmental biology · 2021Article
- Article
- An Alternative Pipeline for Glioblastoma Therapeutics: A Systematic Review of Drug Repurposing in Glioblastoma.Cancers · 2021Review
- Discovery ofMicroorganisms · 2021Article
- Evaluation of Computationally Designed Peptides against TWEAK, a Cytokine of the Tumour Necrosis Factor Ligand Family.International journal of molecular sciences · 2021Article
- A Novel Immune-Related Prognostic Biomarker and Target Associated With Malignant Progression of Glioma.Frontiers in oncology · 2021Article
- Ovarian cancer cells direct monocyte differentiation through a non-canonical pathway.BMC cancer · 2020Article
- Inhibition of Orbivirus Replication by Aurintricarboxylic Acid.International journal of molecular sciences · 2020Article
- Decreased expression of TNFRSF12A in thyroid gland cancer predicts poor prognosis: A study based on TCGA data.Medicine · 2020Observational
Corrections and comments
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Authors and funding
14 authors at 4 institutions in 1 country.
Funding
Abstract
The survival of patients diagnosed with glioblastoma (GBM), the most deadly form of brain cancer, is compromised by the proclivity for local invasion into the surrounding normal brain, which prevents complete surgical resection and contributes to therapeutic resistance. Tumor necrosis factor-like weak inducer of apoptosis (TWEAK), a member of the tumor necrosis factor (TNF) superfamily, can stimulate glioma cell invasion and survival via binding to fibroblast growth factor-inducible 14 (Fn14) and subsequent activation of the transcription factor NF-κB. To discover small molecule inhibitors that disrupt the TWEAK-Fn14 signaling axis, we utilized a cell-based drug-screening assay using HEK293 cells engineered to express both Fn14 and a NF-κB-driven firefly luciferase reporter protein. Focusing on the LOPAC1280 library of 1280 pharmacologically active compounds, we identified aurintricarboxylic acid (ATA) as an agent that suppressed TWEAK-Fn14-NF-κB dependent signaling, but not TNFα-TNFR-NF-κB driven signaling. We demonstrated that ATA repressed TWEAK-induced glioma cell chemotactic migration and invasion via inhibition of Rac1 activation but had no effect on cell viability or Fn14 expression. In addition, ATA treatment enhanced glioma cell sensitivity to both the chemotherapeutic agent temozolomide (TMZ) and radiation-induced cell death. In summary, this work reports a repurposed use of a small molecule inhibitor that targets the TWEAK-Fn14 signaling axis, which could potentially be developed as a new therapeutic agent for treatment of GBM patients.
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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.