ArticleCell death & disease2021
Induction of ferroptosis in human nasopharyngeal cancer cells by cucurbitacin B: molecular mechanism and therapeutic potential.
Article in Cell death & disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
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Who cites it
54 citing papers in PubMed, 92 citations in OpenAlex.
- Pharmacological targeting of ferroptosis in cancer: mechanisms, tumor immunity, and translational challenges.Pharmacological reports : PR · 2026Review
- Subcellular regulation of ferroptosis: roles of individual intracellular organelles and cross talk.American journal of physiology. Cell physiology · 2026Review
- Review
- LINC00839 transcriptionally activated by ELK1 represses ferroptosis in nasopharyngeal carcinoma by regulating UPF1/RCHY1/DJ-1 axis.NPJ precision oncology · 2026Article
- Epithelial-Mesenchymal Transition Shapes the Lipotoxic Response of Colon Cancer Cells to Palmitic Acid.Molecular & cellular proteomics : MCP · 2026Article
- Targeting ferroptosis in cancer: from mechanistic insights to therapeutic approaches.Molecular biomedicine · 2026Review
- Research progress on the regulation of ferroptosis in NPC (Review).Oncology reports · 2026Review
- Cucurbitacin B Inhibits Hepatocellular Carcinoma by Inducing Ferroptosis and Activating the cGAS-STING Pathway.Current issues in molecular biology · 2026Article
- Ferroptosis inhibition and AMPK activation: key mechanisms of soy isoflavones against cerebral injury.Frontiers in immunology · 2026Article
- The COX-2 Inhibitor Celecoxib Sensitizes Nasopharyngeal Carcinoma Cells to Ferroptosis.Current cancer drug targets · 2026Article
- Eupalinolide B exerts cytotoxic effects against KRAS-mutant NSCLC through Nrf2/HO-1-regulated ferroptosis.Acta biochimica et biophysica Sinica · 2025Article
- Targeting Ferroptosis in Nasopharyngeal Carcinoma: Mechanisms, Resistance, and Precision Therapeutic Opportunities.International journal of molecular sciences · 2025Review
- Exploring the antitumor potential of cucurbitacin B in hepatocellular carcinoma through network pharmacology, molecular docking, and molecular dynamics simulations.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Review
- Recent Advances in the Application of Cucurbitacin B as an Anticancer Agent.International journal of molecular sciences · 2025Review
- Solasodine suppresses nasopharyngeal carcinoma progression by inducing ferroptosis.Scientific reports · 2025Article
- TNF-α inhibits Epstein Barr virus reactivation through the GPX4 mediated glutathione pathway.Scientific reports · 2025Article
- Research progress on the use of traditional Chinese medicine to treat diseases by regulating ferroptosis.Genes & diseases · 2025Review
- O-GlcNAc-modified HOXA9 suppresses ferroptosis via promoting UBR5-mediated SIRT6 degradation in nasopharyngeal carcinoma.Neoplasia (New York, N.Y.) · 2025Article
- Therapeutic Approaches with Iron Oxide Nanoparticles to Induce Ferroptosis and Overcome Radioresistance in Cancers.Pharmaceuticals (Basel, Switzerland) · 2025Review
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cucurbitacin B (CuB) is a widely available triterpenoid molecule that exhibits various biological activities. Previous studies on the anti-tumour mechanism of CuB have mostly focused on cell apoptosis, and research on the ferroptosis-inducing effect has rarely been reported. Herein, we first discovered the excellent cytotoxicity of CuB towards human nasopharyngeal carcinoma cells and elucidated its potential ferroptosis-inducing mechanisms. Morphology alterations of mitochondrial ultrastructure, as observed via transmission electron microscopy, showed that CuB-treated cells undergo ferroptosis. CuB caused intracellular accumulation of iron ions and depletion of glutathione. Detailed molecular mechanism investigation confirmed that CuB both induced widespread lipid peroxidation and downregulated the expression of GPX4, ultimately initiating a multipronged mechanism of ferroptosis. Furthermore, CuB exhibited anti-tumour effects in vitro by inhibiting cellular microtubule polymerization, arresting cell cycle and suppressing migration and invasion. Finally, CuB significantly inhibited tumour progression without causing obvious side effects in vivo. Altogether, our study highlighted the therapeutic potential of CuB as a ferroptosis-inducing agent for nasopharyngeal cancer, and it provided valuable insights for developing effective anti-tumour agents with novel molecular mechanisms derived from natural products.
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