ArticleAntioxidants (Basel, Switzerland)2022
Targeting NRF2 Sensitizes Esophageal Adenocarcinoma Cells to Cisplatin through Induction of Ferroptosis and Apoptosis.
Article in Antioxidants (Basel, Switzerland), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed.
- Inhibition or induction of gastrointestinal tumors by ferroptosis and intervention by herbal extracts (Review).Oncology letters · 2026Review
- The role of NRF2 in human cancers: Pre-clinical insights paving the way for clinical trials.Journal of pharmaceutical analysis · 2026Review
- The biology and therapeutic implications of heterogeneity in Barrett oesophagus and oesophageal adenocarcinoma.Nature reviews. Clinical oncology · 2026Review
- Anthocyanin-functionalized selenocysteine nanotherapeutics alleviate cisplatin nephrotoxicity by inhibiting oxidative stress and ferroptosis.Journal of nanobiotechnology · 2025Article
- From Carcinogenesis to Drug Resistance: The Multifaceted Role of Oxidative Stress in Head and Neck Cancer.Cancers · 2025Review
- Antibody-functionalized iron-based nanoplatform for ferroptosis-augmented targeted therapy of HER2-positive breast cancer.Bioactive materials · 2025Article
- Exploring the role of ferroptosis in esophageal cancer: mechanisms and therapeutic implications.Cell death discovery · 2025Review
- Review
- Targeting FTL regulates ferroptosis and remodels lymph node metastasis microenvironment in esophageal squamous cell carcinoma.International journal of biological sciences · 2025Article
- Harnessing the gut microbiome to modulate ferroptosis: a metabolic strategy for the treatment of digestive tract cancers.Frontiers in immunology · 2025Review
- The regulation and function of Nrf2 signaling in ferroptosis-activated cancer therapy.Acta pharmacologica Sinica · 2024Review
- Identification of Penexanthone A as a Novel Chemosensitizer to Induce Ferroptosis by Targeting Nrf2 in Human Colorectal Cancer Cells.Marine drugs · 2024Article
- Oxidative cell death in cancer: mechanisms and therapeutic opportunities.Cell death & disease · 2024Review
- The Role of Nrf2 in the Regulation of Mitochondrial Function and Ferroptosis in Pancreatic Cancer.Antioxidants (Basel, Switzerland) · 2024Review
- Modulators of the Nrf2 Signaling Pathway Enhance the Cytotoxic Effect of Standard Chemotherapeutic Drugs on Organoids of Metastatic Colorectal Cancer.Bulletin of experimental biology and medicine · 2024Article
- Ferroptosis: a new mechanism of traditional Chinese medicine for cancer treatment.Frontiers in pharmacology · 2024Review
- Role of ferroptosis in esophageal cancer and corresponding immunotherapy.World journal of gastrointestinal oncology · 2023Review
- The Transcription Factor NRF2 Has Epigenetic Regulatory Functions Modulating HDACs, DNMTs, and miRNA Biogenesis.Antioxidants (Basel, Switzerland) · 2023Article
- Susceptibility of acute myeloid leukemia cells to ferroptosis and evasion strategies.Frontiers in molecular biosciences · 2023Review
- Unraveling the Complexity of Regulated Cell Death in Esophageal Cancer: from Underlying Mechanisms to Targeted Therapeutics.International journal of biological sciences · 2023Review
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
Esophageal adenocarcinoma (EAC), the predominant type of esophageal cancer in the United States, develops through Barrett's esophagus (BE)-dysplasia-carcinoma cascade. Gastroesophageal reflux disease, where acidic bile salts refluxate into the esophagus, is the main risk factor for the development of BE and its progression to EAC. The NFE2-related factor 2 (NRF2) is the master cellular antioxidant regulator. We detected high NRF2 protein levels in the EAC cell lines and primary tissues. Knockdown of NRF2 significantly enhanced acidic bile salt-induced oxidative stress, DNA damage, and inhibited EAC cell growth. Brusatol, an NRF2 inhibitor, significantly inhibited NRF2 transcriptional activity and downregulated the NRF2 target genes. We discovered that in addition to inducing apoptosis, Brusatol alone or in combination with cisplatin (CDDP) induced significant lipid peroxidation and ferroptosis, as evidenced by reduced xCT and GPX4 expression, two known ferroptosis markers. The combination of Brusatol and CDDP significantly inhibited EAC tumor xenograft growth in vivo and confirmed the in vitro data showing ferroptosis as an important mechanism in the tumors treated with Brusatol or Brusatol and CDDP combination. Our data support the role of NRF2 in protecting against stress-induced apoptosis and ferroptosis in EACs. Targeting NRF2 in combination with platinum therapy can be an effective strategy for eliminating cancer cells in EAC.
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