ArticlePloS one2012
Abortive autophagy induces endoplasmic reticulum stress and cell death in cancer cells.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 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
34 citing papers in PubMed, 47 citations in OpenAlex.
- Distinct roles of COPI proteins attenuated in cell senescence.Science advances · 2026Article
- Interstitial lung disease and the STING pathway.The Journal of clinical investigation · 2026Review
- Fam3C alters Golgi apparatus morphology and function in triple negative breast cancer.Journal of molecular cell biology · 2026Article
- COPG1 Is a Selectively Essential Regulator of Cancer Progression and Chemoresistance via Redox Modulation and AKT Signaling.International journal of molecular sciences · 2026Article
- Expanding the clinical and immunological phenotypes of COPB1 deficiency.Frontiers in immunology · 2026Article
- A new severe congenital neutropenia syndrome associated with autosomal recessive COPZ1 mutations.Blood · 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
- COPZ1: an example of non-oncogene addiction in human tumors.Frontiers in pharmacology · 2025Review
- An updated overview of the search for biomarkers of osteoporosis based on human proteomics.Journal of orthopaedic translation · 2024Review
- Adaptations of membrane trafficking in cancer and tumorigenesis.Journal of cell science · 2024Review
- Heterozygous mutations in the C-terminal domain of COPA underlie a complex autoinflammatory syndrome.The Journal of clinical investigation · 2024Article
- COPI-regulated mitochondria-ER contact site formation maintains axonal integrity.Cell reports · 2023Article
- The role of CaMKK2 in Golgi-associated vesicle trafficking.Biochemical Society transactions · 2023Review
- Impact of interorganelle coordination between the conventional early secretory pathway and autophagy in cellular homeostasis and stress response.Frontiers in cell and developmental biology · 2023Review
- 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
- Secreted protein markers in oral squamous cell carcinoma (OSCC).Clinical proteomics · 2022Article
- Deciphering core proteins of osteoporosis with iron accumulation by proteomics in human bone.Frontiers in endocrinology · 2022Article
- CaMKK2 facilitates Golgi-associated vesicle trafficking to sustain cancer cell proliferation.Cell death & disease · 2021Article
- Article
- Mutations in the COPI coatomer subunit α-COP induce release of Aβ-42 and amyloid precursor protein intracellular domain and increase tau oligomerization and release.Neurobiology of aging · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 1 institution in 1 country.
Funding
Abstract
Autophagic cell death or abortive autophagy has been proposed to eliminate damaged as well as cancer cells, but there remains a critical gap in our knowledge in how this process is regulated. The goal of this study was to identify modulators of the autophagic cell death pathway and elucidate their effects on cellular signaling and function. The result of our siRNA library screenings show that an intact coatomer complex I (COPI) is obligatory for productive autophagy. Depletion of COPI complex members decreased cell survival and impaired productive autophagy which preceded endoplasmic reticulum stress. Further, abortive autophagy provoked by COPI depletion significantly altered growth factor signaling in multiple cancer cell lines. Finally, we show that COPI complex members are overexpressed in an array of cancer cell lines and several types of cancer tissues as compared to normal cell lines or tissues. In cancer tissues, overexpression of COPI members is associated with poor prognosis. Our results demonstrate that the coatomer complex is essential for productive autophagy and cellular survival, and thus inhibition of COPI members may promote cell death of cancer cells when apoptosis is compromised.
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.