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- A 1-year randomized trial of deferasirox alone versus deferasirox and deferoxamine combination for the treatment of iron overload in thalassemia major. [Journal Article]
- TATransfus Apher Sci 2019 Apr 24
- CONCLUSIONS: Our study indicates that combined treatment with deferasirox and deferoxmaine is more effective than deferasirox for reduction of iron over load in patients with thalassemia major.
- Enterobactin, an Iron Chelating Bacterial Siderophore, Arrests Cancer Cell Proliferation. [Journal Article]
- BPBiochem Pharmacol 2019 Jun 19
- Iron is essential for many biological functions, including being a cofactor for enzymes involved in cell proliferation. In line, it has been shown that cancer cells can perturb their iron metabolism …
Iron is essential for many biological functions, including being a cofactor for enzymes involved in cell proliferation. In line, it has been shown that cancer cells can perturb their iron metabolism towards retaining an abundant iron supply for growth and survival. Accordingly, it has been suggested that iron deprivation through the use of iron chelators could attenuate cancer progression. While they have exhibited anti-tumor properties in vitro, the current therapeutic iron chelators are inadequate due to their low efficacy. Therefore, we investigated whether the bacterial catecholate-type siderophore, enterobactin (Ent), could be used as a potent anti-cancer agent given its strong iron chelation property. We demonstrated that iron-free Ent can exert cytotoxic effects specifically towards monocyte-related tumor cell lines (RAW264.7 and J774A.1), but not primary cells, i.e. bone marrow-derived macrophages (BMDMs), through two mechanisms. First, we observed that RAW264.7 and J774A.1 cells preserve a bountiful intracellular labile iron pool (LIP), whose homeostasis can be disrupted by Ent. This may be due, in part, to the lower levels of lipocalin 2 (Lcn2; an Ent-binding protein) in these cell lines, whereas the higher levels of Lcn2 in BMDMs could prevent Ent from hindering their LIP. Secondly, we observed that Ent could dose-dependently impede reactive oxygen species (ROS) generation in the mitochondria. Such disruption in LIP balance and mitochondrial function may in turn promote cancer cell apoptosis. Collectively, our study highlights Ent as an anti-cancer siderophore, which can be exploited as an unique agent for cancer therapy.
- Lecithin-based deferoxamine nanoparticles accelerated cutaneous wound healing in diabetic rats. [Journal Article]
- EJEur J Pharmacol 2019 Jun 19; :172478
- Nanoparticles have higher frequency of being exposed to cells or tissue, and are thus more likely to gain access into cytoplasm or nuclei to modulate molecular events due to significantly larger surf…
Nanoparticles have higher frequency of being exposed to cells or tissue, and are thus more likely to gain access into cytoplasm or nuclei to modulate molecular events due to significantly larger surface area to volume ratio. As a result, they present amplified response or even different physiochemical and biomedical properties from bigger particles. Deferoxamine accelerates wound healing in diabetic rats by increased neovascularization, reduced inflammation and improved maturation of wound. We investigated the wound healing potential of deferoxamine-nanoparticles in diabetic rats. Lecithin based nanoparticles of deferoxamine were prepared and characterized. The diabetic rats were divided into five Groups, of which Group I was treated with pluronic-gel f-127 (25%), Group II with deferoxamine 0.1% and Group III, IV and V were treated with deferoxamine-nanoparticles incorporated in pluronic-gel f-127 25% at 0.03% (0.01% deferoxamine), 0.1% (0.03% deferoxamine) and 0.3% (0.1% deferoxamine) w/v respectively. The wound closure was significantly accelerated in group V as compared to control groups. HIF-1α, VEGF, SDF-1α, TGF-β1, and IL-10 protein levels were significantly higher in group V. The collagen deposition and neovascularization was greater in deferoxamine-nanoparticle treated rats. In contrast, TNF-α level was lowest in group V. In summary, the deferoxamine-nanoparticle formulation we developed, when applied topically on diabetic wounds results in faster wound healing as compared to simple deferoxamine formulation. This formulation may prove to be an effective therapy for treatment of diabetic wounds.
- Iron Deficiency Anemia (IDA) Promotes Visceral Obesity Due to Defective Adipose Tissue Browning (OR09-07-19). [Journal Article]
- CDCurr Dev Nutr 2019; 3(Suppl 1)
- CONCLUSIONS: IDA is an independent risk factor for visceral obesity by decreasing thermogenic energy expenditure.
- NCOA4-Mediated Ferritinophagy Is Essential for HT22 Neuronal Cell Survival During Iron Deficiency (OR15-07-19). [Journal Article]
- CDCurr Dev Nutr 2019; 3(Suppl 1)
- CONCLUSIONS: Our studies demonstrate iron can induce ferroptosis in neuronal cells. We also identify NCOA4-mediated ferritinophagy as an integral process for neuronal cell survival during iron deficiency. Further investigation using multi-omics approaches are in progress to determine the mechanisms by which NCOA4 depletion leads to cell death when extracellular iron supply is limited.
- NCOA4 Mediates Ferritin Responses to Iron, Erythrophagocytosis, and Hepcidin in Macrophages (P24-056-19). [Journal Article]
- CDCurr Dev Nutr 2019; 3(Suppl 1)
- CONCLUSIONS: NCOA4 mediates the release of ferritin iron during cellular iron restriction and iron recycling by macrophages. Moreover, our studies suggest that macrophage NCOA4 is integral to systemic iron homeostasis by responding to the iron regulatory hormone, hepcidin. Thus, NCOA4 and ferritinophagy may potentially serve as therapeutic targets for treatments of iron disorders and anemia of chronic disease.
- Deferoxamine-induced high expression of TfR1 and DMT1 enhanced iron uptake in triple-negative breast cancer cells by activating IL-6/PI3K/AKT pathway. [Journal Article]
- OTOnco Targets Ther 2019; 12:4359-4377
- CONCLUSIONS: We demonstrated that DFO could upregulate expression of TfR1 and DMT1 , which enhanced iron uptake via activating IL-6/PI3K/AKT signaling pathway in aggressive TNBCs.
- New Advances in Evaluation of Hearing in a Sample of Egyptian Children with β-Thalassemia Major. [Journal Article]
- OAOpen Access Maced J Med Sci 2019 May 15; 7(9):1494-1498
- CONCLUSIONS: Hearing loss is prevailing in patients with β-thalassemia major on iron chelating agents. Therefore, regular hearing evaluations and periodic check-ups after the initiation of chelation therapy are mandatory.
- Exosomes Derived from Human Bone Marrow Mesenchymal Stem Cells Stimulated by Deferoxamine Accelerate Cutaneous Wound Healing by Promoting Angiogenesis. [Journal Article]
- BRBiomed Res Int 2019; 2019:9742765
- The exosomes are derived from mesenchymal stem cells (MSCs) and may be potentially used as an alternative for cell therapy, for treating diabetic wounds, and aid in angiogenesis. This study, aimed to…
The exosomes are derived from mesenchymal stem cells (MSCs) and may be potentially used as an alternative for cell therapy, for treating diabetic wounds, and aid in angiogenesis. This study, aimed to investigate whether exosomes originated from bone marrow-derived MSCs (BMSCs) preconditioned by deferoxamine (DFO-Exos) exhibited superior proangiogenic property in wound repair and to explore the underlying mechanisms involved. Human umbilical vein endothelial cells (HUVECs) were used for assays involving cell proliferation, scratch wound healing, and tube formation. To test the effects in vivo, streptozotocin-induced diabetic rats were established. Two weeks after the procedure, histological analysis was used to measure wound-healing effects, and the neovascularization was evaluated as well. Our findings demonstrated that DFO-Exos activate the PI3K/AKT signaling pathway via miR-126 mediated PTEN downregulation to stimulate angiogenesis in vitro. This contributed to enhanced wound healing and angiogenesis in streptozotocin-induced diabetic rats in vivo. Our results suggest that, in cell-free therapies, exosomes derived from DFO preconditioned stem cells manifest increased proangiogenic ability.
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- Synergistic inhibition of tumor cell proliferation by metformin and mito-metformin in the presence of iron chelators. [Journal Article]
- OOncotarget 2019 May 28; 10(37):3518-3532
- We demonstrate that combined treatment with metformin (Met) or its mitochondria-targeted analog, mito-metformin (Mito-Met), and various iron chelators synergistically inhibits proliferation of pancre…
We demonstrate that combined treatment with metformin (Met) or its mitochondria-targeted analog, mito-metformin (Mito-Met), and various iron chelators synergistically inhibits proliferation of pancreatic and triple-negative breast cancer cells. Previously, we reported that Met (at millimolar levels) and Mito-Met (at micromolar levels) inhibited pancreatic cancer cell proliferation. Inhibition of mitochondrial complex I and mitochondrial oxidative phosphorylation (OXPHOS) through stimulation of mitochondrial redox signaling was proposed as a key mechanism for decreased cancer cell proliferation. Because of its poor bioavailability, the use of Met as a "stand-alone" antitumor drug has been questioned. Iron chelators such as deferasirox (DFX) and dexrazoxane (DXR) exhibit antiproliferative effects in cancer cells. The potency of Met and Mito-Met was synergistically enhanced in the presence of iron chelators, DFX, N,N'-bis(2-hydroxyphenyl)ethylendiamine-N,N'-diacetic acid (HBED), and deferoxamine (DFO). Met, DXR (also ICRF-187), and DFO are FDA-approved drugs for treating diabetes, decreasing the incidence and severity of cardiotoxicity following chemotherapy, and mitigating iron toxicity, respectively. Thus, the synergistic antiproliferative effects of Met and Met analogs and iron chelators may have significant clinical relevance in cancer treatment. These findings may have implications in other OXPHOS-mediated cancer therapies.