ReviewCells2024
Benefits and Pitfalls of a Glycosylation Inhibitor Tunicamycin in the Therapeutic Implication of Cancers.
Review in Cells, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
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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.
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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
18 citing papers in PubMed, 15 citations in OpenAlex.
- High-throughput screening system for antimycobacterial compounds usingMicrobiology spectrum · 2026Article
- Structures of Bacterial and Human Phosphoglycosyltransferases Bound to a Common Inhibitor Inform Selective Therapeutics.ACS chemical biology · 2026Article
- New Insights of Muraymycin A1 and Its Analogs as DPAGT1 Inhibitors.Bioorganic chemistry · 2026Article
- Aquatic-derived antimicrobial peptides and their strategically modified analogues as prospective anticancer therapeutics: a comprehensive systematic review of enhancement methodologies and mechanistic insights.Frontiers in chemistry · 2026Review
- Regulation of glycosylation in radiotherapy: exploring the multiple effects of DNA damage, immune response, stromal microenvironment and metabolism.Frontiers in oncology · 2026Review
- Functional inactivation of oligosaccharyltransferase a isoform suppresses tumor metastasis.Glycobiology · 2025Article
- Targeted nanoencapsulation of tunicamycin reduces toxicity while improving its therapeutic effectiveness in pancreatic cancer cells.Molecular therapy. Oncology · 2025Article
- Structures of bacterial and human phosphoglycosyltransferases bound to a common inhibitor inform selective therapeutics.bioRxiv : the preprint server for biology · 2025Article
- Fine-Tuning of the Endoplasmic Reticulum Stress Response Mechanism Plays a Key Role in Cellular Survival-A Mathematical Study.International journal of molecular sciences · 2025Article
- DPAGT1-Perspective as an Anticancer Drug Target.Molecules (Basel, Switzerland) · 2025Review
- Computational Modelling of Tunicamycin C Interaction with Potential Protein Targets: Perspectives from Inverse Docking with Molecular Dynamic Simulation.Current issues in molecular biology · 2025Article
- Sephin1 suppresses ER stress-induced cell death by inhibiting the formation of PP2A holoenzyme.Cell death & disease · 2025Article
- Farnesol Improves Endoplasmic Reticulum Stress and Hepatic Metabolic Dysfunction Induced by Tunicamycin in Mice.Biology · 2025Article
- TunR2, a novel mode-of-action tunicamycin-type antibiotic: Pharmacokinetics in C57BL/6 mouse and Holstein cattle.PloS one · 2025Article
- Spring viraemia of carp virus modulates the time-dependent unfolded protein response to facilitate viral replication.Frontiers in immunology · 2025Article
- STK33 as the functional substrate of miR-454-3p for suppression and apoptosis in neuroblastoma.Molecules and cells · 2024Article
- Chimeras Derived from a P2YACS pharmacology & translational science · 2024Article
- Enhancement of Triple-Negative Breast Cancer-Specific Induction of Cell Death by Silver Nanoparticles by Combined Treatment with Proteotoxic Stress Response Inhibitors.Nanomaterials (Basel, Switzerland) · 2024Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
The aberrant glycosylation is a hallmark of cancer progression and chemoresistance. It is also an immune therapeutic target for various cancers. Tunicamycin (TM) is one of the potent nucleoside antibiotics and an inhibitor of aberrant glycosylation in various cancer cells, including breast cancer, gastric cancer, and pancreatic cancer, parallel with the inhibition of cancer cell growth and progression of tumors. Like chemotherapies such as doxorubicin (DOX), 5'fluorouracil, etoposide, and cisplatin, TM induces the unfolded protein response (UPR) by blocking aberrant glycosylation. Consequently, stress is induced in the endoplasmic reticulum (ER) that promotes apoptosis. TM can thus be considered a potent antitumor drug in various cancers and may promote chemosensitivity. However, its lack of cell-type-specific cytotoxicity impedes its anticancer efficacy. In this review, we focus on recent advances in our understanding of the benefits and pitfalls of TM therapies in various cancers, including breast, colon, and pancreatic cancers, and discuss the mechanisms identified by which TM functions. Finally, we discuss the potential use of nano-based drug delivery systems to overcome non-specific toxicity and enhance the therapeutic efficacy of TM as a targeted therapy.
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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.