ArticleCell death discovery2021
CCAAT/Enhancer-binding protein delta mediates glioma stem-like cell enrichment and ATP-binding cassette transporter ABCA1 activation for temozolomide resistance in glioblastoma.
Article in Cell death discovery, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
What it found
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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
25 citing papers in PubMed.
- CCAAT/enhancer-binding protein delta regulates miRs-4257 and 3156 to attenuate the interleukin 12 through small extracellular vesicle transmission in glioblastoma.Cancer cell international · 2026Article
- Machine learning-integrated network toxicology uncovers glioma targets of DEHP.Frontiers in toxicology · 2026Article
- Research progress on glioma drug resistance: mechanism analysis and therapeutic strategies.Frontiers in pharmacology · 2026Review
- GTSE1-expressed osteoblastic cells facilitate formation of pro-metastatic tumor microenvironment in osteosarcoma.Genes & diseases · 2025Article
- APOL4-mediated intracellular cholesterol trafficking is essential for glioblastoma cell growth.BMC cancer · 2025Article
- Basic biology and roles of CEBPD in cardiovascular disease.Cell death discovery · 2025Review
- Enhancer reprogramming: critical roles in cancer and promising therapeutic strategies.Cell death discovery · 2025Review
- Transcription Factor CEBPD-Mediated WTAP Facilitates the Stemness, Growth, Migration and Glycolysis of Glioblastoma Stem Like Cells.Neurochemical research · 2025Article
- A novel Tc17 population recruited by tumor cells promotes tumor progression in gastric cancer.Frontiers in oncology · 2025Article
- Single-cell/spatial integration reveals an MES2-like glioblastoma program orchestrated by immune communication and regulatory networks.Frontiers in immunology · 2025Article
- A pan-cancer analysis targeting the oncogenic role of ATP-binding cassette transporter A1 in human tumors.Frontiers in oncology · 2025Review
- Amantadine against glioma via ROS-mediated apoptosis and autophagy arrest.Cell death & disease · 2024Article
- Article
- Titanium dioxide nanostructure-loaded Adriamycin surmounts resistance in breast cancer therapy: ABCA/P53/C-myc crosstalk.Future science OA · 2024Article
- Drug metabolism-related gene ABCA1 augments temozolomide chemoresistance and immune infiltration abundance of M2 macrophages in glioma.European journal of medical research · 2023Article
- Coixendide efficacy in combination with temozolomide in glioblastoma and transcriptome analysis of the mechanism.Scientific reports · 2023Article
- Review
- Review
- The biological impacts of CEBPD on urothelial carcinoma development and progression.Frontiers in oncology · 2023Review
- Inhibition of MZF1/c-MYC Axis by Cantharidin Impairs Cell Proliferation in Glioblastoma.International journal of molecular sciences · 2022Article
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
Glioblastoma (GBM) is the most aggressive brain tumor and relapses after chemo- or radiotherapy in a short time. The anticancer drug temozolamide (TMZ) is commonly used for GBM treatment, but glioma stem-like cells (GSCs) often lead to drug resistance and therapeutic failure. To date, the mechanism of GSC formation in TMZ-treated GBM remains largely unknown. CCAAT/Enhancer-binding protein delta (CEBPD) is an inflammation-responsive transcription factor and is proposed to be oncogenic in the context of drug resistance, prompting us to clarify its role in TMZ-resistant GBM. In this study, we first found that the CEBPD protein levels in GBM patients were significantly increased and further contributed to TMZ resistance by promoting GSC formation. Accordingly, the protein levels of stemness transcription factors, namely, SRY-box transcription factor 2 (SOX2), octamer-binding transcription factor 4 (OCT4), NANOG, and ATP-binding cassette subfamily A member 1 (ABCA1), were increased in GSCs and TMZ-treated GBM cells. Increased binding of CEBPD to promoter regions was observed in GSCs, indicating the direct regulation of these GSC-related genes by CEBPD. In addition, an ABCA1 inhibitor increased the caspase 3/7 activity of TMZ-treated GSCs, suggesting that TMZ efflux is controlled by ABCA1 activity and that the expression levels of the ABCA1 gene are an indicator of the efficiency of TMZ treatment. Together, we revealed the mechanism of CEBPD-mediated GSC drug resistance and proposed ABCA1 inhibition as a potential strategy for the treatment of TMZ-resistant GBM.
Identifiers
What Socratic 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 Socratic graph.