ArticleJournal of experimental & clinical cancer research : CR2018
Lipid accumulation in human breast cancer cells injured by iron depletors.
Article in Journal of experimental & clinical cancer research : CR, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 25 citations in OpenAlex.
- Article
- Thiosemicarbazide Derivative of Captopril (8) imposes Cellular-Dependent Death Modalities on Breast Cancer Cell Lines.Asian Pacific journal of cancer prevention : APJCP · 2025Article
- Exosomes derived from umbilical cord blood NK cells inhibit the progression of pancreatic cancer by targeting ROS-mediated mitochondrial dysfunction.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2025Article
- Iron, Ferroptosis, and Head and Neck Cancer.International journal of molecular sciences · 2023Review
- Investigating ionizing radiation-induced changes in breast cancer cells using stimulated Raman scattering microscopy.Journal of biomedical optics · 2023Article
- Reduced sulfatide content in deferoxamine-induced senescent HepG2 cells.The international journal of biochemistry & cell biology · 2023Article
- Comprehensive Analysis of Prognosis and Immune Landscapes Based on Lipid-Metabolism- and Ferroptosis-Associated Signature in Uterine Corpus Endometrial Carcinoma.Diagnostics (Basel, Switzerland) · 2023Article
- Article
- Double-edge sword roles of iron in driving energy production versus instigating ferroptosis.Cell death & disease · 2022Review
- Novel iron chelator SK4 demonstrates cytotoxicity in a range of tumour derived cell lines.Frontiers in molecular biosciences · 2022Article
- Lipid droplets and ferritin heavy chain: a devilish liaison in human cancer cell radioresistance.eLife · 2021Article
- Reversing oncogenic transformation with iron chelation.Oncotarget · 2021Review
- Dp44mT, an iron chelator, suppresses growth and induces apoptosis via RORA-mediated NDRG2-IL6/JAK2/STAT3 signaling in glioma.Cellular oncology (Dordrecht, Netherlands) · 2020Article
- Nonlinear Optical Microscopy: From Fundamentals to Applications in Live Bioimaging.Frontiers in bioengineering and biotechnology · 2020Review
- In Vitro Toxicity Assessment of Stilbene Extract for Its Potential Use as Antioxidant in the Wine Industry.Antioxidants (Basel, Switzerland) · 2019Article
- Synergistic inhibition of tumor cell proliferation by metformin and mito-metformin in the presence of iron chelators.Oncotarget · 2019Article
- New Water-Soluble Copper(II) Complexes with Morpholine-Thiosemicarbazone Hybrids: Insights into the Anticancer and Antibacterial Mode of Action.Journal of medicinal chemistry · 2019Article
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Authors and funding
10 authors at 5 institutions in 1 country.
Funding
Abstract
backgroundCurrent insights into the effects of iron deficiency in tumour cells are not commensurate with the importance of iron in cell metabolism. Studies have predominantly focused on the effects of oxygen or glucose scarcity in tumour cells, while attributing insufficient emphasis to the inadequate supply of iron in hypoxic regions. Cellular responses to iron deficiency and hypoxia are interlinked and may strongly affect tumour metabolism.
methodsWe examined the morphological, proteomic, and metabolic effects induced by two iron chelators-deferoxamine (DFO) and di-2-pyridylketone 4,4-dimethyl-3-thiosemicarbazone (Dp44mT)-on MDA-MB-231 and MDA-MB-157 breast cancer cells.
resultsThese chelators induced a cytoplasmic massive vacuolation and accumulation of lipid droplets (LDs), eventually followed by implosive, non-autophagic, and non-apoptotic death similar to methuosis. Vacuoles and LDs are generated by expansion of the endoplasmic reticulum (ER) based on extracellular fluid import, which includes unsaturated fatty acids that accumulate in LDs. Typical physiological phenomena associated with hypoxia are observed, such as inhibition of translation, mitochondrial dysfunction, and metabolic remodelling. These survival-oriented changes are associated with a greater expression of epithelial/mesenchymal transcription markers.
conclusionsIron starvation induces a hypoxia-like program able to scavenge nutrients from the extracellular environment, and cells assume a hypertrophic phenotype. Such survival strategy is accompanied by the ER-dependent massive cytoplasmic vacuolization, mitochondrial dysfunctions, and LD accumulation and then evolves into cell death. LDs containing a greater proportion of unsaturated lipids are released as a consequence of cell death. The consequence of the disruption of iron metabolism in tumour tissue and the effects of LDs on intercellular communication, cancer-inflammation axis, and immunity remain to be explored. Considering the potential benefits, these are crucial subjects for future mechanistic and clinical studies.
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