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Tumors hijack macrophages for iron supply to promote bone metastasis and anemia

ABSTRACT: Tumors hijack macrophages for iron supply to promote bone metastasis and anemia

PROVIDER: PRJNA1129146 | ENA |

REPOSITORIES: ENA

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Tumors hijack macrophages for iron supply to promote bone metastasis and anemia

Project description:This SuperSeries is composed of the SubSeries listed below.

2025-08-20 | GSE270983 | GEO

Cardiac transcriptome in iron-deficiency anemia

Project description:Purpose: The goal of this study was to probe for the effects of iron-deficiency anemia on the cardiac transciprtome using RNA-seq Methods: C57B6 mice were weaned onto a control or iron-deficient diet for 6 weeks. Hearts were removed and total mRNA was submitted for RNA-seq. Sequencing data was aligned using STAR and differetial gene expression analysis conducted in R using EdgeR and DESeq2. qRT–PCR validation for genes of interest was performed using TaqMan and SYBR Green assays. Results: We mapped about 24 million sequence reads per sample to the mouse genome (build mm10) and identified 13,590 transcripts in the hearts of control and iron-deficient mice after removing lowly expressed genes and PCR duplicates. Differential gene expression analysis showed approximately 78% downregulated and 22% upregulated genes in iron-deficiency anemia compared to controls. PCA plot showed control and iron-deficient hearts clustering in two distinct and separate clusters. Conclusions: Our study represents the first whole-transcriptomic study on cardiac samples obtained from iron-deficient and anemic mice, with biologic replicates, generated by RNA-seq technology. The RNA-seq data presented here can be used by others to explore which pathways are affected by iron-deficiency anemia

2020-12-03 | GSE162493 | GEO

Cardiac transcriptome in iron-deficiency anemia

Project description:Cardiac transcriptome in iron-deficiency anemia

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Viruses hijack FPN1 to disrupt iron withholding and suppress host defense

Project description:Iron withholding controls infections by limiting the pathogens’ access to iron from the host. Viruses directly utilize intracellular materials, including iron, to complete their life cycles. Emerging evidence suggests the importance of withholding iron in limiting viral infections. However, the mechanisms through which viruses disrupt host iron homeostasis and the impact of intracellular iron on the host’s antiviral defense remain unknown. Here we show that viral infections facilitate the polyubiquitination and degradation of ferroportin (FPN1, the only cellular iron exporter) by upregulating the host E3 ubiquitin ligase DTX3L, leading to an elevation in cellular iron levels. Excessive ferrous suppresses type I IFN responses and autophagy by promoting TBK1 hydroxylation and STING carbonylation in macrophages. FPN1 deficiency suppresses host antiviral defense and facilitates viral replication in vitro and in vivo, while DTX3L deficiency has the opposite effect. These results reveal that viruses hijack host FPN1 to disrupt iron withholding and achieve immune escape, and suggest that iron homeostasis maintained by FPN1 is required for the optimal activation of TBK1- and STING-dependent antiviral responses.

2025-01-01 | GSE280144 | GEO

Iron Therapy in Colo-Rectal Neoplasm and Iron Deficiency Anemia: Intravenous Iron Sucrose Versus Oral Ferrous Sulphate.

Project description:The main objective of this study is to evaluate the efficacy of intravenous iron sucrose in increasing preoperative haemoglobin values in patients with colo-rectal neoplasm and iron deficiency anemia, compared to the standard treatment with oral iron. It will also determine whether intravenous iron sucrose administration improves outcomes such as postoperative haemoglobin values, serum ferritin values, transfusional needs, postoperative complications, or length of hospital stay.

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Usefulness of Fecal Immunochemical Test in Iron Deficiency Anemia (IDAFIT)

Project description:Prospective study to test whether the immunochemical fecal occult blood test (FIT) for colorectal cancer (CRC) helps to prioritize patients with iron deficiency anemia for colonoscopy.

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Iron deficiency anemia in mice involves alterations in mitophagy and gene expression in erythroblasts

Project description:Since iron deficiency anemia (IDA) is one of the most common diseases in worldwide, it is an essential issue to prevent and to treat the IDA in public healthcare system. However, the precise adaptive responses and their mechanisms of the hematopoietic system induced by iron deficient state are not fully understood. In this study, low iron diet conditions which induce sever iron deficiency anemia in mice were established. Transcriptome analyses in erythroblasts under normal or iron deficient states were performed to describe the pathological details of IDA. Under iron deficient state, extensive gene expression changes and mitophagy disorder were induced during the terminal maturation of erythroblasts. These findings provide a new insight into pathophysiology and molecular biology of IDA and the function of iron as a coordinator of gene expression networks in erythrocyte maturation.

2016-12-14 | GSE77694 | GEO

fe-fit-diff_6d-Differential gene expression in A. thaliana roots depending on iron supply and FIT (FER-LIKE IRON DEFICIENCY-INDUCED TRANSCRIPTION FACTOR) abundance

Project description:au15-01_iron-fit - fe-fit-diff_6d - Changes in gene expression profiles between fit knock-out, wild-type and FIT overexpressor seedlings under sufficient iron supply and under iron deficiency. - Col-0, HA-FIT and fit-3.

2016-07-01 | GSE80281 | GEO

Effects of Preoperative Correction of Anemia With Intravenously Iron in Colorectal Cancer Patients.

Project description:The aim of the study is to examine the effects of anemia correction with intravenous administered iron on clinical outcomes and the immune response on the tumor in patients with planned colonic- or rectal cancer surgery. The study will be performed as a retrospective propensity score-matched cohort study with an examination of immune response in tumor and clinical outcomes, between patients with anemia without correction with iron(III)isomaltoside, non-anemic patients, and anemic patients treated with iron(III)isomaltoside prior to surgery. Propensity score matching will ensure identification of controls from a pool of patients treated at the Department of Surgery, Zealand University Hospital. The two control groups will be: an anemic historical control group (group 1), and a non-anemic concurrent control group (group 2). Group 3 will be the treatment group, with patients with anemia and treated with iron(III)isomaltoside. The study period of cases undergoing i.v. treatment will be 1st of February 2017 to 31st of October 2019 with approximately 70 cases included

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Viruses hijack FPN1 to disrupt iron withholding and suppress host defense

Project description:Viruses hijack FPN1 to disrupt iron withholding and suppress host defense

| PRJNA1176542 | ENA