ArticleOncogene2021
Loss of COPZ1 induces NCOA4 mediated autophagy and ferroptosis in glioblastoma cell lines.
Article in Oncogene, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 114 papers.
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Who cites it
114 citing papers in PubMed, 203 citations in OpenAlex.
- PROTACs in cancer therapy: targeted degradation of GPX4, PARP and epigenetic regulators.Journal of enzyme inhibition and medicinal chemistry · 2026Review
- COPZ1 depletion induces cell death through different mechanisms in in vitro murine models of thyroid cancer.European thyroid journal · 2026Article
- HIF-1α/HO-1 Axis Promotes Ferroptosis and Impairs Periodontal Tissue Repair in Periodontitis.Journal of clinical periodontology · 2026Article
- Pin1 targets phosphorylated NCOA4 for K29/K48-linked ubiquitination to suppress ferritinophagy and ferroptosis in anaplastic thyroid cancer.Cell death & disease · 2026Article
- A fistful of iron: ferritin as a vulnerability point of the brain cancers.Cell death & disease · 2026Review
- Targeting dormant cancer cells: ferroptosis as a precision therapeutic strategy.Cellular & molecular biology letters · 2026Review
- Targeting ferroptosis in cancer: from mechanistic insights to therapeutic approaches.Molecular biomedicine · 2026Review
- Ferroptosis in Glioblastoma and Neuroblastoma: Molecular Mechanisms and Novel Therapeutic Strategies.Current issues in molecular biology · 2026Review
- Cancer neuroscience: signaling pathways and new therapeutic strategies for cancer.Signal transduction and targeted therapy · 2026Review
- Defining treatment-resistant brain cancer: Genetic screening to identify oncogene-driven immunomodulation and therapy resistance.Cancer gene therapy · 2026Review
- Parallel Single-Tissue Summary-Data Mendelian Randomization and Functional Validation Identify the ARRDC1 Promoter SNP rs4494021 as a Genetic Marker Associated with Anxiety Disorders.Neuropsychiatric disease and treatment · 2026Article
- Biochemical and Comparative Proteomic Analyses Delineate the Anti-Ovarian Carcinogenic Roles of Modified Calycosin.Food science & nutrition · 2026Article
- Identification of COPZ1 as a Shared Candidate Ferroptosis-Related Hub Gene in Periodontitis and Inflammatory Bowel Disease.Human mutation · 2026Article
- NCOA4 as a regulatory switch linking DNA damage to lipid peroxidation in radiation response.Frontiers in cell and developmental biology · 2026Review
- Dauricine Inhibits Macrophages M2 Polarization and Regulates the Progression and Ferroptosis via HCK/IDO1 in Urinary Bladder Cancer.Food science & nutrition · 2025Article
- Harnessing ferroptosis to transform glioblastoma therapy and surmount treatment resistance.Cell death discovery · 2025Review
- Regulation of iron metabolism in ferroptosis: From mechanism research to clinical translation.Journal of pharmaceutical analysis · 2025Review
- Identification of prognostic biomarkers in colorectal cancer through multi-omics profiling of programmed cell death pathways.Journal of gastrointestinal oncology · 2025Article
- Ioning out glioblastoma: ferroptosis mechanisms and therapeutic frontiers.Cell death discovery · 2025Review
- Clinical significance of NCOA4 in glioblastoma: diagnostic, prognostic, and therapeutic value.BMC cancer · 2025Article
54 more citing papers are in PubMed but not listed here.
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Authors and funding
18 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Dysregulated iron metabolism is a hallmark of many cancers, including glioblastoma (GBM). However, its role in tumor progression remains unclear. Herein, we identified coatomer protein complex subunit zeta 1 (COPZ1) as a therapeutic target candidate which significantly dysregulated iron metabolism in GBM cells. Overexpression of COPZ1 was associated with increasing tumor grade and poor prognosis in glioma patients based on analysis of expression data from the publicly available database The Cancer Genome Atlas (P < 0.001). Protein levels of COPZ1 were significantly increased in GBM compared to non-neoplastic brain tissue samples in immunohistochemistry and western blot analysis. SiRNA knockdown of COPZ1 suppressed proliferation of U87MG, U251 and P3#GBM in vitro. Stable expression of a COPZ1 shRNA construct in U87MG inhibited tumor growth in vivo by ~60% relative to controls at day 21 after implantation (P < 0.001). Kaplan-Meier analysis of the survival data demonstrated that the overall survival of tumor bearing animals increased from 20.8 days (control) to 27.8 days (knockdown, P < 0.05). COPZ1 knockdown also led to the increase in nuclear receptor coactivator 4 (NCOA4), resulting in the degradation of ferritin, and a subsequent increase in the intracellular levels of ferrous iron and ultimately ferroptosis. These data demonstrate that COPZ1 is a critical mediator in iron metabolism. The COPZ1/NCOA4/FTH1 axis is therefore a novel therapeutic target for the treatment of human GBM.
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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.