ArticleAntioxidants & redox signaling2019
Effects of Ferroportin-Mediated Iron Depletion in Cells Representative of Different Histological Subtypes of Prostate Cancer.
Article in Antioxidants & redox signaling, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 47 citations in OpenAlex.
- Review
- Crosstalk between ferroptosis and endoplasmic reticulum stress: A potential target for ovarian cancer therapy (Review).International journal of molecular medicine · 2025Review
- Nanoparticle-Mediated Ferroptosis for Cancer Therapy: Mechanisms and Therapeutic Strategies.Nanotechnology, science and applications · 2025Review
- Sulforaphane inhibits multiple myeloma cell-induced osteoclast differentiation and macrophage proliferation by elevating ferroportin1.Cancer chemotherapy and pharmacology · 2024Article
- Redox-Regulated Iron Metabolism and Ferroptosis in Ovarian Cancer: Molecular Insights and Therapeutic Opportunities.Antioxidants (Basel, Switzerland) · 2024Review
- Transcriptional regulation of genetic variants in theThe Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2024Article
- In vivo bioluminescence imaging of labile iron in xenograft models and liver using FeAL-1, an iron-activatable form of D-luciferin.Cell chemical biology · 2023Article
- Distinct functions between ferrous and ferric iron in lung cancer cell growth.Cancer science · 2023Article
- Assessing the Potential of Small Peptides for Altering Expression Levels of the Iron-Regulatory GenesInternational journal of molecular sciences · 2023Article
- Review
- Ferroptosis landscape in prostate cancer from molecular and metabolic perspective.Cell death discovery · 2023Review
- Relevant Membrane Transport Proteins as Possible Gatekeepers for Effective Pharmacological Ascorbate Treatment in Cancer.Antioxidants (Basel, Switzerland) · 2023Review
- Elevated labile iron in castration-resistant prostate cancer is targetable with ferrous iron-activatable antiandrogen therapy.European journal of medicinal chemistry · 2023Article
- Highly Metastatic Subpopulation of TNBC Cells Has Limited Iron Metabolism and Is a Target of Iron Chelators.Cancers · 2023Article
- Role of dietary iron revisited: in metabolism, ferroptosis and pathophysiology of cancer.American journal of cancer research · 2022Review
- The protective effects of Pimavanserin against cerebral ischemia-induced brain injury.Bioengineered · 2021Article
- Downregulation of FPN1 acts as a prognostic biomarker associated with immune infiltration in lung cancer.Aging · 2021Article
- Nrf2 Is a Potential Modulator for Orchestrating Iron Homeostasis and Redox Balance in Cancer Cells.Frontiers in cell and developmental biology · 2021Article
- The role of iron homeostasis and iron-mediated ROS in cancer.American journal of cancer research · 2021Review
- The Role of Iron in Cancer Progression.Frontiers in oncology · 2021Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
aimsFerroportin (FPN) is an iron exporter that plays an important role in cellular and systemic iron metabolism. Our previous work has demonstrated that FPN is decreased in prostate tumors. We sought to identify the molecular pathways regulated by FPN in prostate cancer cells.
resultsWe show that overexpression of FPN induces profound effects in cells representative of multiple histological subtypes of prostate cancer by activating different but converging pathways. Induction of FPN induces autophagy and activates the transcription factors tumor protein 53 (p53) and Kruppel-like factor 6 (KLF6) and their common downstream target, cyclin-dependent kinase inhibitor 1A (p21). FPN also induces cell cycle arrest and stress-induced DNA-damage genes. Effects of FPN are attributable to its effects on intracellular iron and can be reproduced with iron chelators. Importantly, expression of FPN not only inhibits proliferation of all prostate cancer cells studied but also reduces growth of tumors derived from castrate-resistant adenocarcinoma C4-2 cells in vivo. INNOVATION: We use a novel model of FPN expression to interrogate molecular pathways triggered by iron depletion in prostate cancer cells. Since prostate cancer encompasses different subtypes with a highly variable clinical course, we further explore how histopathological subtype influences the response to iron depletion. We demonstrate that prostate cancer cells that derive from different histopathological subtypes activate converging pathways in response to FPN-mediated iron depletion. Activation of these pathways is sufficient to significantly reduce the growth of treatment-refractory C4-2 prostate tumors in vivo.
conclusionsOur results may explain why FPN is dramatically suppressed in cancer cells, and they suggest that FPN agonists may be beneficial in the treatment of prostate cancer.
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