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Iron chelation therapy elicits innate immune control of metastatic ovarian cancer

ABSTRACT: Iron chelation therapy elicits innate immune control of metastatic ovarian cancer

PROVIDER: PRJNA1031179 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26484730_1.fastq.gz	Fastqsanger.gz
	SRR26484730_2.fastq.gz	Fastqsanger.gz
	SRR26484731_1.fastq.gz	Fastqsanger.gz
	SRR26484731_2.fastq.gz	Fastqsanger.gz
	SRR26484732_1.fastq.gz	Fastqsanger.gz

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Iron chelation therapy elicits innate immune control of metastatic ovarian cancer

Project description:Iron accumulation in cancer cells contributes to malignant progression and chemoresistance. While disrupting this process can influence various hallmarks of cancer, the immunomodulatory effects of chelating iron in tumors remain undefined. Here, we report that treatment with deferiprone, an FDA-approved iron chelator, elicits innate immune responses that control metastatic ovarian cancer. Deferiprone reprogrammed ovarian cancer cells towards an immunostimulatory state characterized by enhanced production of type I interferon (IFN) and surface overexpression of molecules that activate natural killer (NK) cells. Mechanistically, this reprogramming was driven by innate sensing of mitochondrial DNA in the cytosol and concomitant activation of nuclear DNA damage responses evoked upon iron chelation. Deferiprone administration synergized with chemotherapy and prolonged the survival of mice bearing metastatic ovarian cancer by bolstering intratumoral NK cell infiltration and type I IFN responses. Iron chelation may represent an alternative immunotherapeutic approach for malignancies that are normally refractory to T cell-centric modalities.

2024-06-26 | GSE246051 | GEO

Iron chelation shifts endothelial phenotypes

Project description:Iron deficiency is a highly prevalent nutrient deficiency and the most common cause of anemia. Although iron deficiency exacerbates cardiovascular disease, the direct impact of iron deficiency on the vasculature remains unstudied. Human lymphatic and arterial endothelial cells were treated with deferoxamine for 24 hours to assess the impact of iron deficiency on endothelial cell phenotypes. We found iron chelation upregulated the expression of arterial makers in both cell types. In lymphatic endothelial cells, iron chelation decreased the expression of lymphatic markers. These data suggest iron chelation shifts endothelial cells toward an arterial phenotype.

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Iron chelation shifts endothelial phenotypes

Project description:Iron chelation shifts endothelial phenotypes

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Change expression of genes in iron chelation and deficient conditions

Project description:Change expression of genes in iron chelation and deficient conditions

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A co-conserved gene pair supports Caulobacter iron homeostasis and resistance to chelation stress

Project description:Bacteria assimilate a diverse set of metals that enable metabolic functions essential for growth and survival, but metal homeostasis can be disrupted by natural and synthetic chelators in the environment. We have identified genes that influence fitness of the common soil and aquatic bacterium, Caulobacter crescentus, in the presence of a growth-limiting concentration of the synthetic chelator ethylenediaminetetraacetic acid (EDTA). Among the identified genes important in EDTAacclimationthere are several controlled by the metal-responsive regulators Fur, Zur, and UzcRS. However, a subset of genes in the iron-responsive Fur regulon emerged as the primary fitness determinants during EDTA challenge. EDTA treatment reduced intracellular iron levels and a syntenic gene pair, cciT and cciO, that supports Caulobacter iron homeostasis is necessary for growth in EDTA. cciT encodes one of four Fur-regulated TonB-dependent transporters (TBDTs) and – of these regulators – uniquely supports wild-type levels of growth on defined and complex lab media. The iron acquisition and EDTA resistance functions of the CciT transporter specifically require the presence of cciO, which encodes a 2-oxoglutarate-Fe(II) dioxygenase. Thus, there is a critical functional partnership between an outer membrane transporter and a cytoplasmic dioxygenase that are broadly co-conserved in the phylum Proteobacteria. cciT and cciO mutants cultivated in natural freshwater were not impacted by an equivalent EDTA treatment, demonstrating robustness of the highly redundant set of Caulobacter iron acquisition systems in an ecosystem context. This study advances our understanding of genes involved in metal acquisition and chelation stress survival, and illuminates the complex interactions between the chemical environment and the processes that regulate intracellular metal homeostasis.

2024-08-14 | GSE274268 | GEO

Heme Deficient vs Wild Type in Low Iron

Project description:Heme Deficient or Wild Type (normal heme) for 6 hrs with iron chelation by BPS. Keywords: Cell Type Comparison

2005-10-18 | GSE3470 | GEO

Treatment of a human lymphoblastoid cell line with the iron chelator deferoxamine

Project description:We treated lymphoblast cells with the iron chelator deferoxamine (DFO) for 60 hours to determine if iron chelation would affect the levels of intron lariats.

2022-03-23 | GSE199077 | GEO

A co-conserved gene pair supports Caulobacter iron homeostasis and resistance to chelation stress

Project description:A co-conserved gene pair supports Caulobacter iron homeostasis and resistance to chelation stress

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Change expression of genes in iron chelation and deficient conditions

Project description:Firstly, cell senescence and anti-oxidant genes were down-regulated by iron deficient mice and iron-specific chelator deferoxamine (DFO) using a DNA microarray. Our data suggested that down-regulation of anti-oxidant genes and cell senescence gene induced oxidative stress in iron-deficient and -specific chelated condition.

2018-01-26 | GSE109656 | GEO

Iron Chelators Treatment on DMS-53 Human Lung Cancer Cell

Project description:The molecular role of iron in gene expression remains poorly characterized. Moreover, the alterations in global gene expression after iron chelation remains unclear and are important to assess for understanding the molecular pathology of iron-depletion and the biological effects of iron chelators. We assessed the effect on whole genome gene expression of two iron chelators (desferrioxamine and Dp44mT). These studies are important for understanding the molecular and cellular effects of iron-depletion.

2011-12-31 | GSE26920 | GEO

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