ArticleCell death & disease2024
Cancer-associated fibroblasts secrete FGF5 to inhibit ferroptosis to decrease cisplatin sensitivity in nasopharyngeal carcinoma through binding to FGFR2.
Article in Cell death & disease, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 28 citations in OpenAlex.
- RHBDD2 Confers Insensitivity of Esophageal Squamous Cell Carcinoma to Cisplatin by Inhibiting Ferroptosis Through the Wnt3a/β-Catenin/FTH1 Axis.Cell biochemistry and biophysics · 2026Article
- Single-cell sequencing reveals an immunotherapy-relevant IFITM1-marked epithelial interferon state in nasopharyngeal carcinoma.Translational oncology · 2026Article
- Co-Culture of nasopharyngeal carcinoma cells and fibroblasts induces altered integrin expression associated with 3D structural formation.Cytotechnology · 2026Article
- Inducing Ferroptosis: Sensitization Strategy for Radiotherapy and Its Application.Antioxidants (Basel, Switzerland) · 2026Review
- Research progress on the regulation of ferroptosis in NPC (Review).Oncology reports · 2026Review
- Cancer-associated fibroblasts: enablers of tumor drug resistance.Journal of translational medicine · 2026Review
- FGF19 in Solid Tumors: Molecular Mechanisms, Metabolic Reprogramming, and Emerging Therapeutic Opportunities.Theranostics · 2026Review
- Targeting Ferroptosis in Nasopharyngeal Carcinoma: Mechanisms, Resistance, and Precision Therapeutic Opportunities.International journal of molecular sciences · 2025Review
- Ropivacaine-loaded tumor-derived vesicles targeting CCNB1 and autophagy in nasopharyngeal carcinoma.Materials today. Bio · 2025Article
- Ferroptosis and Nrf2 Signaling in Head and Neck Cancer: Resistance Mechanisms and Therapeutic Prospects.Antioxidants (Basel, Switzerland) · 2025Review
- Heme oxygenase-1 leads to cisplatin resistance in nasopharyngeal carcinoma by reducing oxidative stress and ferroptosis.Cancer cell international · 2025Article
- Ferroptosis in cancer: revealing the multifaceted functions of mitochondria.Cellular and molecular life sciences : CMLS · 2025Review
- Solasodine suppresses nasopharyngeal carcinoma progression by inducing ferroptosis.Scientific reports · 2025Article
- Integrating Bulk and Single-Cell Transcriptomics with Machine Learning Reveals a Heme Metabolism-Based Panel for Lung Adenocarcinoma Chemotherapy Resistance.International journal of molecular sciences · 2025Article
- O-GlcNAc-modified HOXA9 suppresses ferroptosis via promoting UBR5-mediated SIRT6 degradation in nasopharyngeal carcinoma.Neoplasia (New York, N.Y.) · 2025Article
- Multi-Omics Characterization of Genome-Wide Abnormal DNA Methylation Reveals FGF5 as a Diagnosis of Nasopharyngeal Carcinoma Recurrence After Radiotherapy.Biomolecules · 2025Article
- Cancer-associated fibroblasts: dual roles from senescence sentinels to death regulators and new dimensions in therapy.Frontiers in immunology · 2025Review
- Pan-cancer analysis reveals MTTP as a prognostic and immunotherapeutic biomarker in human tumors.Frontiers in immunology · 2025Article
- Cancer associated fibroblasts in tumors: focusing on solid tumors and hematological malignancies.Frontiers in oncology · 2025Review
- Role of N6-methyladenosine methylation in nasopharyngeal carcinoma: current insights and future prospective.Cell death discovery · 2024Review
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cisplatin (DDP)-based chemoradiotherapy is one of the standard treatments for nasopharyngeal carcinoma (NPC). However, the sensitivity and side effects of DDP to patients remain major obstacles for NPC treatment. This research aimed to study DDP sensitivity regulated by cancer-associated fibroblasts (CAFs) through modulating ferroptosis. We demonstrated that DDP triggered ferroptosis in NPC cells, and it inhibited tumor growth via inducing ferroptosis in xenograft model. CAFs secreted high level of FGF5, thus inhibiting DDP-induced ferroptosis in NPC cells. Mechanistically, FGF5 secreted by CAFs directly bound to FGFR2 in NPC cells, leading to the activation of Keap1/Nrf2/HO-1 signaling. Rescued experiments indicated that FGFR2 overexpression inhibited DDP-induced ferroptosis, and CAFs protected against DDP-induced ferroptosis via FGF5/FGFR2 axis in NPC cells. In vivo data further showed the protective effects of FGF5 on DDP-triggered ferroptosis in NPC xenograft model. In conclusion, CAFs inhibited ferroptosis to decrease DDP sensitivity in NPC through secreting FGF5 and activating downstream FGFR2/Nrf2 signaling. The therapeutic strategy targeting FGF5/FGFR2 axis from CAFs might augment DDP sensitivity, thus decreasing the side effects of DDP in NPC treatment.
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