ArticleOxidative medicine and cellular longevity2022
CCAAT/Enhancer-Binding Protein Delta Regulates Glioblastoma Survival through Catalase-Mediated Hydrogen Peroxide Clearance.
Article in Oxidative medicine and cellular longevity, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Redox Regulation in Glioblastoma: Mechanisms, Biomarkers, and Therapeutic Implications.International journal of molecular sciences · 2026Review
- Development of an AAPH-Induced Oxidative Stress Model in Bovine Mammary Epithelial Cells and Investigation of Its Molecular Mechanisms.Antioxidants (Basel, Switzerland) · 2026Article
- A Janus Amyloid-like Nanofilm Inhibits Colorectal Cancer Postoperative Recurrence and Abdominal Adhesion via Synergistic Enzyme Cascade.Nanomaterials (Basel, Switzerland) · 2025Article
- Basic biology and roles of CEBPD in cardiovascular disease.Cell death discovery · 2025Review
- EMB-driven glioblastoma multiforme progression via the MCT4/GPX3 axis: therapeutic inhibition by Ganxintriol A.Journal of translational medicine · 2025Article
- Comprehensive analysis of biological landscape of oxidative stress-related genes in diabetic erectile dysfunction.International journal of impotence research · 2024Article
- CCAAT enhancer binding protein delta activates vesicle associated membrane protein 3 transcription to enhance chemoresistance and extracellular PD-L1 expression in triple-negative breast cancer.Journal of experimental & clinical cancer research : CR · 2024Article
- First-in-Class Dual EZH2-HSP90 Inhibitor Eliciting Striking Antiglioblastoma ActivityJournal of medicinal chemistry · 2024Article
- Review
- ROS regulation in gliomas: implications for treatment strategies.Frontiers in immunology · 2023Review
Corrections and comments
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Authors and funding
8 authors.
Funding
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Abstract
It has long been documented that cancer cells show increased and persistent oxidative stress due to increased reactive oxygen species (ROS), which is necessary for their increased proliferative rate. Due to the high levels of ROS, cancer cells also stimulate the antioxidant system, which includes the enzymes superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPX), to eliminate ROS. However, overexpressed antioxidant enzymes often lead to drug resistance and therapeutic failure. Glioblastoma (GBM) is the most aggressive brain tumor and has the poorest prognosis. The transcription factor CCAAT/enhancer-binding protein delta (CEBPD) is highly expressed in GBM and correlates with drug resistance, prompting us to elucidate its role in GBM cell survival. In this study, we first demonstrated that loss of CEBPD significantly inhibited GBM cell viability and increased cell apoptosis. Furthermore, the expression of CAT was attenuated through promoter regulation following CEBPD knockdown, accelerating intracellular hydrogen peroxide (H
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