ReviewFrontiers in pharmacology2025
COPZ1: an example of non-oncogene addiction in human tumors.
Review in Frontiers in pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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
1 citing paper in PubMed.
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Non-oncogene addiction (NOA) indicates that tumor cell growth/survival requires the activity of genes/pathways not oncogenic per sé, and dispensable for normal cells. NOA genes provide a wide repertoire of novel therapeutic exploitable tumor vulnerabilities. A large body of evidence demonstrates the dependency of several tumors such as breast, prostate, ovary, thyroid, glioblastoma and LUAD, on the activity of COPZ1, a component of the heptameric COPI complex. Thus, COPZ1 is emerging as a potential novel therapeutic target for tumors of different origin. In different tumor models COPZ1 inhibition was found implicated in abortive autophagy, ER stress and activation of ferroptosis. In this review we summarize the different studies characterizing COPZ1 as a NOA gene in different tumor types, and discuss potential issues related to its targeting.
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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.