ArticleJournal of experimental & clinical cancer research : CR2018
Tunicamycin specifically aggravates ER stress and overcomes chemoresistance in multidrug-resistant gastric cancer cells by inhibiting N-glycosylation.
Article in Journal of experimental & clinical cancer research : CR, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 128 papers.
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Who cites it
128 citing papers in PubMed, 212 citations in OpenAlex.
- Unraveling the Mechanisms of Chemoresistance in Gastric Cancer: Insights and Emerging Research Strategies.Current oncology reports · 2026Review
- Article
- Iron-endoplasmic reticulum-extracellular matrix axis regulates cancer cell invasion.bioRxiv : the preprint server for biology · 2026Article
- Remodelling the tumour microenvironment and beyond: ERO1A as a multifaceted regulator and emerging therapeutic target in cancer.Clinical and translational medicine · 2026Review
- Modulatory Activity of Uncaria tomentosa Extract in the Expression of Proteins Involved in the Unfolded Protein Response and Insulin Resistance.Current issues in molecular biology · 2026Article
- The OAS1-FASN axis promotes pancreatic cancer by coordinating lipogenic stress and the unfolded protein response.Cell death & disease · 2026Article
- Calcineurin-responsive zinc finger 1 (Crz1) contributes to stress tolerance and virulence in the pathogenic fungusInfection and immunity · 2026Article
- HOOK2 downregulation compromises the tumorigenic and stemness properties of ovarian cancer cells by increasing endoplasmic reticulum stress.Cell death & disease · 2026Article
- Disruption of spike protein N-glycosylation induces its endoplasmic reticulum retention and attenuates SARS-CoV-2 infectivity.Journal of virology · 2026Article
- Endoplasmic reticulum stress in disease pathogenesis: its implications for therapy.Signal transduction and targeted therapy · 2026Review
- ER stress affects proliferation and induces polyploidization of cultured human HaCaT and A431 cells.Histochemistry and cell biology · 2026Article
- An Evaluation of the Interaction of Brefeldin A with Mitogen-Activated Protein Kinase 1 (MAPK1) and Protein Kinase C Alpha (PrKCα): Insights from Molecular Modelling Studies.International journal of molecular sciences · 2026Article
- Heat shock factor-1 alleviates ER-stress in Caenorhabditis elegans.Scientific reports · 2026Article
- Ferulic Acid Alleviates Chemotherapy-Induced POI by Targeting the Grp78 and Perk-eIF2α-ATF4-CHOP Pathway to Attenuate Endoplasmic Reticulum Stress.Biomedicines · 2026Article
- Identification of isoform switching events linked with esophageal adenocarcinoma patient survival informs novel prognostic and therapeutic targets.Cell death & disease · 2026Article
- Poly(ADP-ribose) glycohydrolase enforces p21 degradation via dePARylation to promote gastric cancer progression.The Journal of clinical investigation · 2026Article
- Mannose metabolic pathway senses glucose supply and regulates cell fate decisions.The Journal of biological chemistry · 2026Article
- Axin1 stabilizes S-opsin and maintains cone photoreceptor survival by inhibiting GSK3β activity.Cell death discovery · 2026Article
- Targeted nanoencapsulation of tunicamycin reduces toxicity while improving its therapeutic effectiveness in pancreatic cancer cells.Molecular therapy. Oncology · 2025Article
- Imaginal discs produce neuropeptide-like precursor 1 to alleviate ER stress in response to warm temperatures.Communications biology · 2025Article
68 more citing papers are in PubMed but not listed here.
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundMultidrug resistance remains a major obstacle to successful treatment for patients with gastric cancer (GC). Recently, glycosylation has been demonstrated to play a vital role in the acquisition of multidrug resistance. As a potent inhibitor of glycosylation, tunicamycin (Tu) has shown marked antitumor activities in various cancers. In the present study, we attempted to determine the exact effect of Tu on the chemoresistance of GC.
methodsThe cytotoxic effects of drugs on GC cells were evaluated by cell viability assays, and apoptosis was detected by flow cytometry. PCR, western blot analysis, immunofluorescence staining and canonical inhibitors were employed to identify the underlying mechanisms of the specific effects of Tu on multidrug-resistant (MDR) GC cells.
resultsFor the first time, we found that MDR GC cells were more sensitive to Tu-induced cell death than the parental cells and that the increased sensitivity might correlate with basal endoplasmic reticulum (ER) stress. In addition, Tu dramatically increased chemotherapy-induced apoptosis by evoking ER stress in GC cells, particularly MDR cells. Further study indicated that these effects were highly dependent on glycosylation inhibition by Tu, rather than its role as a canonical ER stress inducer. Besides, autophagy was markedly triggered by Tu, and blocking autophagy enhanced the combined effects of Tu and chemotherapy on MDR GC cells.
conclusionsOur results suggest that tumor-targeted glycosylation inhibition may be a feasible strategy to reverse chemoresistance in GC patients.
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