ArticleRedox biology2020
Epigenetic reprogramming of epithelial-mesenchymal transition promotes ferroptosis of head and neck cancer.
Article in Redox biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 134 papers.
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Who cites it
134 citing papers in PubMed, 224 citations in OpenAlex.
- Ferroptosis-related stress during aging and its relevance to disease.GeroScience · 2026Review
- Opposing roles of DGAT-mediated lipid droplet biogenesis in the regulation of ferroptosis sensitivity.The FEBS journal · 2026Article
- Inhibition of EphA2 triggers ferroptosis by disrupting USP38mediated SLC7A11 stabilization in chemoresistant gastric cancer.Cellular and molecular life sciences : CMLS · 2026Article
- Non-coding RNAs as master regulators of ferroptosis in cancer: mechanisms and clinical implications.Molecular cancer · 2026Review
- Unveiling the molecular landscape: Long non-coding RNAs in neuroblastoma (Review).Oncology reports · 2026Review
- Understanding and Exploiting Biological Mechanisms of Radiosensitization Using High Atomic Mass Nanomaterials.Nanomaterials (Basel, Switzerland) · 2026Review
- Ferroptosis as a therapeutic target in cancer: mechanisms, immune interactions, and emerging strategies.Molecular cancer · 2026Review
- Cell adhesion molecules as emerging regulators of ferroptosis: mechanisms and therapeutic opportunities in cancer.Apoptosis : an international journal on programmed cell death · 2026Review
- Ferritin as a novel predictive index for nasopharyngeal carcinoma survival and therapeutic efficacy of different chemotherapy regimens.World journal of clinical oncology · 2026Article
- Emerging Role of Sirtuins-Mediated Ferroptosis in Hepatocellular Carcinoma Progression: Mechanisms and Therapeutic Perspectives.Journal of hepatocellular carcinoma · 2026Review
- CBX3 promotes epithelial-mesenchymal transition in synovial sarcoma via the SHH signaling pathway.American journal of cancer research · 2026Article
- Ferroptosis in biliary tract cancer: Molecular mechanisms and therapeutic applications (Review).International journal of oncology · 2026Review
- M6A-ALKBH5-dependent RBMS3-AS3 down-regulation suppresses ferroptosis to promote lung adenocarcinoma progression through HNRNPDL/ZEB1/GPX4 axis.NPJ precision oncology · 2025Article
- Ferroptosis and head and neck cancer: Mechanisms and therapeutic perspectives (Review).International journal of molecular medicine · 2025Review
- ZEB1 and Uveal Melanoma Invasiveness.International journal of molecular sciences · 2025Article
- Activation of a FOXO3-induced cell cycle arrest regulates ferroptosis.Cell death discovery · 2025Article
- Integration of machine learning to reveal the correlation between ferroptosis and M2 macrophages in head and neck squamous cell carcinoma.Discover oncology · 2025Article
- β-elemene promotes ferroptosis to improve the sensitivity of imatinib in gastrointestinal stromal tumours by targeting N6AMT1.Clinical and translational medicine · 2025Article
- Transcriptional activation of PHKG2 by TP53 promotes ferroptosis through nuclear export of NRF2 in head and neck squamous cell carcinoma.Cell death & disease · 2025Article
- GATA3 promotes ferroptosis resistance by repressing integrin β1 signaling.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
74 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ferroptosis is a newly defined form of cell death induced by iron-dependent accumulation of lethal lipid peroxidation. Ferroptosis represent a therapeutic strategy to suppress therapy-resistant cancer cells with more property of epithelial-mesenchymal transition (EMT). However, epigenetic reprogramming of EMT has been rarely studied in the context of ferroptosis susceptibility. Therefore, we examined the therapeutic potentiality of EMT epigenetic reprogramming in promoting ferroptosis in head and neck cancer (HNC) cells. The effects of ferroptosis inducers and EMT inhibition or induction were tested in HNC cell lines and mouse tumor xenograft models. These effects were analyzed concerning cell viability and death, lipid reactive oxygen species and iron production, labile iron pool, glutathione contents, NAD/NADH levels, and mRNA/protein expression. Cell density and the expression levels of E-cadherin, vimentin, and ZEB1 were associated with the different susceptibility to ferroptosis inducers. CDH1 silencing or ZEB1 overexpression increased the susceptibility to ferroptosis, whereas CDH overexpression or ZEB1 silencing decreased the susceptibility, in vitro and in vivo. Histone deacetylase SIRT1 gene silencing or pharmacological inhibition by EX-527 suppressed EMT and consequently decreased ferroptosis, whereas SIRT inducers, resveratrol and SRT1720, increased ferroptosis. MiR-200 family inhibitors induced EMT and increased ferroptosis susceptibility. In HNC cells with low expression of E-cadherin, the treatment of 5-azacitidine diminished the hypermethylation of CDH1, resulting in increased E-cadherin expression and decreased ferroptosis susceptibility. Our data suggest that epigenetic reprogramming of EMT contributes to promoting ferroptosis in HNC cells.
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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.