ArticleProceedings of the National Academy of Sciences of the United States of America2011
Tumor-specific silencing of COPZ2 gene encoding coatomer protein complex subunit ζ 2 renders tumor cells dependent on its paralogous gene COPZ1.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 60 citations in OpenAlex.
- COPI Coatomer Regulates Several Steps of HDL Metabolism.Arteriosclerosis, thrombosis, and vascular biology · 2026Article
- COPZ1 depletion induces cell death through different mechanisms in in vitro murine models of thyroid cancer.European thyroid journal · 2026Article
- Proteomic maps of synapses and synaptic vesicles across the central and enteric nervous systems.Communications biology · 2026Article
- The COPI coatomer influences LDL receptor activity, hepatic lipid storage, and apoB secretion.bioRxiv : the preprint server for biology · 2026Article
- Fam3C alters Golgi apparatus morphology and function in triple negative breast cancer.Journal of molecular cell biology · 2026Article
- Scalable and accurate rare-variant association tests for whole genome sequencing time-to-event analysis in large biobanks.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- COPG1 Is a Selectively Essential Regulator of Cancer Progression and Chemoresistance via Redox Modulation and AKT Signaling.International journal of molecular sciences · 2026Article
- Coding and regulatory somatic profiling of triple-negative breast cancer in Sub-Saharan African patients.Scientific reports · 2025Article
- COPZ1: an example of non-oncogene addiction in human tumors.Frontiers in pharmacology · 2025Review
- Chemoproteomics enables identification of coatomer subunit zeta-1 targeted by a small molecule for enterovirus A71 inhibition.MedComm · 2024Article
- Adaptations of membrane trafficking in cancer and tumorigenesis.Journal of cell science · 2024Review
- High expression of COPZ2 is associated with poor prognosis and cancer progression in glioma.Frontiers in molecular neuroscience · 2024Article
- A Comprehensive Pan-Cancer Analysis of the Regulation and Prognostic Effect of Coat Complex Subunit Zeta 1.Genes · 2023Article
- Depletion of COPI in cancer cells: the role of reactive oxygen species in the induction of lipid accumulation, noncanonical lipophagy and apoptosis.Molecular biology of the cell · 2022Article
- Differential Involvement ofCells · 2022Article
- Article
- CaMKK2 facilitates Golgi-associated vesicle trafficking to sustain cancer cell proliferation.Cell death & disease · 2021Article
- Nanogel-facilitated Protein Intracellular Specific Degradation through Trim-Away.Advanced functional materials · 2021Article
- Loss of COPZ1 induces NCOA4 mediated autophagy and ferroptosis in glioblastoma cell lines.Oncogene · 2021Article
- High-Dimensional Mediation Analysis Based on Additive Hazards Model for Survival Data.Frontiers in genetics · 2021Article
Corrections and comments
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Authors and funding
13 authors at 4 institutions in 2 countries.
Funding
Abstract
Anticancer drugs are effective against tumors that depend on the molecular target of the drug. Known targets of cytotoxic anticancer drugs are involved in cell proliferation; drugs acting on such targets are ineffective against nonproliferating tumor cells, survival of which leads to eventual therapy failure. Function-based genomic screening identified the coatomer protein complex ζ1 (COPZ1) gene as essential for different tumor cell types but not for normal cells. COPZ1 encodes a subunit of coatomer protein complex 1 (COPI) involved in intracellular traffic and autophagy. The knockdown of COPZ1, but not of COPZ2 encoding isoform coatomer protein complex ζ2, caused Golgi apparatus collapse, blocked autophagy, and induced apoptosis in both proliferating and nondividing tumor cells. In contrast, inhibition of normal cell growth required simultaneous knockdown of both COPZ1 and COPZ2. COPZ2 (but not COPZ1) was down-regulated in the majority of tumor cell lines and in clinical samples of different cancer types. Reexpression of COPZ2 protected tumor cells from killing by COPZ1 knockdown, indicating that tumor cell dependence on COPZ1 is the result of COPZ2 silencing. COPZ2 displays no tumor-suppressive activities, but it harbors microRNA 152, which is silenced in tumor cells concurrently with COPZ2 and acts as a tumor suppressor in vitro and in vivo. Silencing of microRNA 152 in different cancers and the ensuing down-regulation of its host gene COPZ2 offer a therapeutic opportunity for proliferation-independent selective killing of tumor cells by COPZ1-targeting agents.
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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.