ArticleInternational journal of molecular sciences2018
Thioredoxin Confers Intrinsic Resistance to Cytostatic Drugs in Human Glioma Cells.
Article in International journal of molecular sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 26 citations in OpenAlex.
- Redox rewiring in glioblastoma: the thioredoxin system as a precision therapeutic target.Pharmacological reports : PR · 2026Review
- Inhibitory Effect of TrxR Inhibitor Ag (Ⅰ) Schiff Base Complex Against Cervical Cancer Via ROS-mediated ASK1/MAPK Signaling and Autophagy.Biological trace element research · 2026Article
- Metabolic drivers of genome instability in cancer: mechanisms and therapeutic opportunities.Experimental hematology & oncology · 2026Review
- The Role of Se-Containing Glutathione Peroxidases and Thioredoxin Reductases in Oncogenesis: Expression Paradoxes and Therapeutic Prospects.Antioxidants (Basel, Switzerland) · 2026Review
- Exploring the Role of Thioredoxin system in Cancer Immunotherapy.Journal of Cancer · 2025Article
- Synergistic Dual Targeting of Thioredoxin and Glutathione Systems Irrespective of p53 in Glioblastoma Stem Cells.Antioxidants (Basel, Switzerland) · 2024Article
- Article
- The role of TXNIP in cancer: a fine balance between redox, metabolic, and immunological tumor control.British journal of cancer · 2023Review
- The Role of the Thioredoxin Detoxification System in Cancer Progression and Resistance.Frontiers in molecular biosciences · 2022Review
- Cisplatin Resistance and Redox-Metabolic Vulnerability: A Second Alteration.International journal of molecular sciences · 2021Review
- Cytotoxic, chemosensitizing and radiosensitizing effects of curcumin based on thioredoxin system inhibition in breast cancer cells: 2D vs. 3D cell culture system.Experimental and therapeutic medicine · 2021Article
- Elucidating Role of Reactive Oxygen Species (ROS) in Cisplatin Chemotherapy: A Focus on Molecular Pathways and Possible Therapeutic Strategies.Molecules (Basel, Switzerland) · 2021Review
- Pathogenic role of the SP/ NK1R system in GBM cells through inhibiting the thioredoxin system.Iranian journal of basic medical sciences · 2021Article
- Nucleoredoxin Knockdown in SH-SY5Y Cells Promotes Cell Renewal.Antioxidants (Basel, Switzerland) · 2021Article
- Metallothionein-3 promotes cisplatin chemoresistance remodelling in neuroblastoma.Scientific reports · 2021Article
- Uronic acid metabolic process-related gene expression-based signature predicts overall survival of glioma.Bioscience reports · 2021Article
- Drug Resistance in Glioblastoma: The Two Faces of Oxidative Stress.Frontiers in molecular biosciences · 2020Review
- Natural Sesquiterpene Lactones Enhance Chemosensitivity of Tumor Cells through Redox Regulation of STAT3 Signaling.Oxidative medicine and cellular longevity · 2019Review
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Thioredoxin (Trx) overexpression is known to be a cause of chemotherapy resistance in various tumor entities. However, Trx effects on resistance are complex and depend strictly on tissue type. In the present study, we analyzed the impact of the Trx system on intrinsic chemoresistance of human glioblastoma multiforme (GBM) cells to cytostatic drugs. Resistance of GBM cell lines and primary cells to drugs and signaling inhibitors was assessed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assays. Impact of Trx inhibition on apoptosis was investigated by proteome profiling of a subset of proteins and annexin V apoptosis assays. Trx-interacting protein (TXNIP) was overexpressed by transfection and protein expression was determined by immunoblotting. Pharmacological inhibition of Trx by 1-methyl-2-imidazolyl-disulfide (PX-12) reduced viability of three GBM cell lines, induced expression of active caspase-3, and reduced phosphorylation of AKT-kinase and expression of β-catenin. Sensitivity to cisplatin could be restored by both PX-12 and recombinant expression of the upstream Trx inhibitor TXNIP, respectively. In addition, PX-12 also sensitized primary human GBM cells to temozolomide. Combined inhibition of Trx and the phosphatidylinositide 3-kinase (PI3K) pathway resulted in massive cell death. We conclude that the Trx system and the PI3K pathway act as a sequential cascade and could potentially present a new drug target.
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