ArticleMolecular biology of the cell2022
Depletion of COPI in cancer cells: the role of reactive oxygen species in the induction of lipid accumulation, noncanonical lipophagy and apoptosis.
Article in Molecular biology of the cell, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
13 citing papers in PubMed, 14 citations in OpenAlex.
- COPZ1 depletion induces cell death through different mechanisms in in vitro murine models of thyroid cancer.European thyroid journal · 2026Article
- COPG1 Is a Selectively Essential Regulator of Cancer Progression and Chemoresistance via Redox Modulation and AKT Signaling.International journal of molecular sciences · 2026Article
- Single-particle tracking of genetically encoded nanoparticles: Optimizing expression for cytoplasmic diffusion studies.Biophysical journal · 2025Article
- PSP205, a Novel Phenyl Sulfonyl Piperidine, Induces Apoptotic Cell Death in Colon Cancer by Modulating Coat Protein Complex-Mediated Vesicle Trafficking.ACS pharmacology & translational science · 2025Article
- COPB1 deficiency triggers osteoporosis with elevated iron stores by inducing osteoblast ferroptosis.Journal of orthopaedic translation · 2025Article
- Identification of a Fetal De Novo Splice Variant inMaternal-fetal medicine (Wolters Kluwer Health, Inc.) · 2025Article
- COPZ1: an example of non-oncogene addiction in human tumors.Frontiers in pharmacology · 2025Review
- Adaptations of membrane trafficking in cancer and tumorigenesis.Journal of cell science · 2024Review
- Butyrate increases methylglyoxal production through regulation of the JAK2/Stat3/Nrf2/Glo1 pathway in castration‑resistant prostate cancer cells.Oncology reports · 2024Article
- COPI Vesicle Disruption Inhibits Mineralization via mTORC1-Mediated Autophagy.International journal of molecular sciences · 2023Article
- Arf1 coordinates fatty acid metabolism and mitochondrial homeostasis.Nature cell biology · 2023Article
- Defects in lipid homeostasis reflect the function of TANGO2 in phospholipid and neutral lipid metabolism.eLife · 2023Article
- The role of CaMKK2 in Golgi-associated vesicle trafficking.Biochemical Society transactions · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 3 institutions in 1 country.
Funding
Abstract
The coatomer protein complex 1 (COPI) is a multisubunit complex that coats intracellular vesicles and is involved in intracellular protein trafficking. Recently we and others found that depletion of COPI complex subunits zeta (COPZ1) and delta (ARCN1) preferentially kills tumor cells relative to normal cells. Here we delineate the specific cellular effects and sequence of events of COPI complex depletion in tumor cells. We find that this depletion leads to the inhibition of mitochondrial oxidative phosphorylation and the elevation of reactive oxygen species (ROS) production, followed by accumulation of lipid droplets (LDs) and autophagy-associated proteins LC3-II and SQSTM1/p62 and, finally, apoptosis of the tumor cells. Inactivation of ROS in COPI-depleted cells with the mitochondrial-specific quencher, mitoquinone mesylate, attenuated apoptosis and markedly decreased both the size and the number of LDs. COPI depletion caused ROS-dependent accumulation of LC3-II and SQSTM1 which colocalizes with LDs. Lack of double-membrane autophagosomes and insensitivity to Atg5 deletion suggested an accumulation of a microlipophagy complex on the surface of LDs induced by depletion of the COPI complex. Our findings suggest a sequence of cellular events triggered by COPI depletion, starting with inhibition of oxidative phosphorylation, followed by ROS activation and accumulation of LDs and apoptosis.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.