ArticleInternational journal of molecular sciences2018
Chemoresistance in H-Ferritin Silenced Cells: The Role of NF-κB.
Article in International journal of molecular sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 14 citations in OpenAlex.
- Acute Exposure to Cadmium Triggers NCOA4-Mediated Ferritinophagy and Ferroptosis in Never-Smokers Oral Cancer Cells.International journal of biological sciences · 2025Article
- A novel view of ferritin in cancer.Biochimica et biophysica acta. Reviews on cancer · 2023Review
- Ferroptosis as an emerging target in rheumatoid arthritis.Frontiers in immunology · 2023Review
- Ferroptosis and its emerging role in esophageal cancer.Frontiers in molecular biosciences · 2022Review
- Ferritin heavy chain (FTH1) exerts significant antigrowth effects in breast cancer cells by inhibiting the expression of c-MYC.FEBS open bio · 2021Article
- FTH1 Pseudogenes in Cancer and Cell Metabolism.Cells · 2020Review
- Review
- FtH-Mediated ROS Dysregulation Promotes CXCL12/CXCR4 Axis Activation and EMT-Like Trans-Differentiation in Erythroleukemia K562 Cells.Frontiers in oncology · 2020Article
- Magnetoferritin: Process, Prospects, and Their Biomedical Applications.International journal of molecular sciences · 2019Review
- H-Ferritin Affects Cisplatin-Induced Cytotoxicity in Ovarian Cancer Cells through the Modulation of ROS.Oxidative medicine and cellular longevity · 2019Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nuclear Factor-κB (NF-κB) is frequently activated in tumor cells contributing to aggressive tumor growth and resistance to chemotherapy. Here we demonstrate that Ferritin Heavy Chain (FHC) protein expression inversely correlates with NF-κB activation in cancer cell lines. In fact, FHC silencing in K562 and SKOV3 cancer cell lines induced p65 nuclear accumulation, whereas FHC overexpression correlated with p65 nuclear depletion in the same cell lines. In FHC-silenced cells, the p65 nuclear accumulation was reverted by treatment with the reactive oxygen species (ROS) scavenger, indicating that NF-κB activation was an indirect effect of FHC on redox metabolism. Finally, FHC knock-down in K562 and SKOV3 cancer cell lines resulted in an improved cell viability following doxorubicin or cisplatin treatment, being counteracted by the transient expression of inhibitory of NF-κB, IκBα. Our results provide an additional layer of information on the complex interplay of FHC with cellular metabolism, and highlight a novel scenario of NF-κB-mediated chemoresistance triggered by the downregulation of FHC with potential therapeutic implications.
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Registered trials
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