ArticleCell death & disease2014
Combination therapy targeting ectopic ATP synthase and 26S proteasome induces ER stress in breast cancer cells.
Article in Cell death & disease, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.
What it found
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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
28 citing papers in PubMed, 1 synthesis or guideline pooled it, 44 citations in OpenAlex.
- FMolecular biology reports · 2023Pooled it
- Surface Complex V couples proton gradient across the plasma membrane to ATP production in cancer.Research square · 2026Article
- Surface Complex V couples proton gradient across the plasma membrane to ATP production in cancer.bioRxiv : the preprint server for biology · 2026Article
- The Histone Deacetylase HstD Regulates Fungal Growth, Development and Secondary Metabolite Biosynthesis inInternational journal of molecular sciences · 2023Article
- Ectopic ATP synthase stimulates the secretion of extracellular vesicles in cancer cells.Communications biology · 2023Article
- Spatial and temporal dynamics of ATP synthase from mitochondria toward the cell surface.Communications biology · 2023Article
- Induction of Secondary Metabolite Biosynthesis by Deleting the Histone Deacetylase HdaA in the Marine-Derived FungusJournal of fungi (Basel, Switzerland) · 2022Article
- Beneficial effect of polyphenols in COVID-19 and the ectopic FJournal of cellular biochemistry · 2022Article
- Review
- Defueling the cancer: ATP synthase as an emerging target in cancer therapy.Molecular therapy oncolytics · 2021Review
- Proteomic Analysis Reveals That Metformin Suppresses PSMD2, STIP1, and CAP1 for Preventing Gastric Cancer AGS Cell Proliferation and Migration.ACS omega · 2021Article
- The function of Cav-1 in MDA-MB-231 breast cancer cell migration and invasion induced by ectopic ATP5B.Medical oncology (Northwood, London, England) · 2021Article
- From Pinocytosis to Methuosis-Fluid Consumption as a Risk Factor for Cell Death.Frontiers in cell and developmental biology · 2021Review
- Natural products and other inhibitors of FEuropean journal of medicinal chemistry · 2020Review
- Multiomics Reveals Ectopic ATP Synthase Blockade Induces Cancer Cell Death via a lncRNA-mediated Phospho-signaling Network.Molecular & cellular proteomics : MCP · 2020Article
- Targeting breast cancer metabolism with a novel inhibitor of mitochondrial ATP synthesis.Oncotarget · 2020Article
- Review
- Recent advances in the genome mining ofMedChemComm · 2019Review
- Discovery and Elucidation of the Biosynthesis of Aspernidgulenes: Novel Polyenes from Aspergillus Nidulans by Using Serial Promoter Replacement.Chembiochem : a European journal of chemical biology · 2019Article
- Positioning of proteasome inhibitors in therapy of solid malignancies.Cancer chemotherapy and pharmacology · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
F1Fo ATP synthase is present in all organisms and is predominantly located on the inner membrane of mitochondria in eukaryotic cells. The present study demonstrated that ATP synthase and electron transport chain complexes were ectopically expressed on the surface of breast cancer cells and could serve as a potent anticancer target. We investigated the anticancer effects of the ATP synthase inhibitor citreoviridin on breast cancer cells through proteomic approaches and revealed that differentially expressed proteins in cell cycle regulation and in the unfolded protein response were functionally enriched. We showed that citreoviridin triggered PERK-mediated eIF2α phosphorylation, which in turn attenuated general protein synthesis and led to cell cycle arrest in the G0/G1 phase. We further showed that the combination of citreoviridin and the 26S proteasome inhibitor bortezomib could improve the anticancer activity by enhancing ER stress, by ameliorating citreoviridin-caused cyclin D3 compensation, and by contributing to CDK1 deactivation and PCNA downregulation. More interestingly, the combined treatment triggered lethality through unusual non-apoptotic caspase- and autophagy-independent cell death with a cytoplasmic vacuolization phenotype. The results imply that by boosting ER stress, the combination of ATP synthase inhibitor citreoviridin and 26S proteasome inhibitor bortezomib could potentially be an effective therapeutic strategy against breast cancer.
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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 OpenQuestion graph.