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Critical Role of Ferritin-Mediated Iron Homeostasis in the Maintenance of Hematopoietic Stem Cells and Leukemia Stem Cells

ABSTRACT: Critical Role of Ferritin-Mediated Iron Homeostasis in the Maintenance of Hematopoietic Stem Cells and Leukemia Stem Cells

PROVIDER: PRJNA1005185 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25629345_1.fastq.gz	Fastqsanger.gz
	SRR25629345_2.fastq.gz	Fastqsanger.gz
	SRR25629346_1.fastq.gz	Fastqsanger.gz
	SRR25629346_2.fastq.gz	Fastqsanger.gz
	SRR25629347_1.fastq.gz	Fastqsanger.gz

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Critical Role of Ferritin-Mediated Iron Homeostasis in the Maintenance of Hematopoietic Stem Cells and Leukemia Stem Cells

Project description:Iron metabolism has emerged as a critical factor in cell viability, both in normal and pathological contexts. However, the intricate relationship between iron metabolism and the maintenance of adult stem cells and cancer stem cells remains incompletely understood. The ferritin complex, responsible for intracellular iron storage and buffering, plays a pivotal role in this process. Our research provides insights into the regulatory role of ferritin-mediated iron homeostasis in hematopoietic stem cells (HSCs).

2024-04-17 | GSE240742 | GEO

Glial ferritin maintains self-renewal and proliferation of neural stem cells by supplying iron in Drosophila

Project description:Stem cell niche is critical for regulating the behavior of stem cells. Drosophila neural stem cells (Neuroblasts, NBs) are encased by glial niche cells closely, but it still remains unclear whether glial niche cells can regulate the self-renewal and differentiation of NBs. Here we show that ferritin produced by glia, cooperates with Zip13 to transport iron into NBs for the energy production, which is essential to the self-renewal and proliferation of NBs. The knockdown of glial ferritin encoding genes causes energy shortage in NBs, which leads to the low proliferation and premature differentiation of NBs. Moreover, the level of glial ferritin production is affected by the status of NBs, establishing a bicellular iron homeostasis. In this study, we demonstrate that glial cells are indispensable to maintain the self-renewal of NBs, unveiling a novel role of the NB glial niche during brain development.

2024-07-15 | GSE237124 | GEO

Gene Expression by array after Ferritin Knockdown in Preferential Iron Trafficking Characterizes Glioblastoma Stem-like Cells

Project description:Glioblastomas display hierarchies with self-renewing cancer stem-like cells (CSCs). RNA sequencing and enhancer mapping revealed regulatory programs unique to CSCs causing upregulation of the iron transporter transferrin, the top differentially expressed gene compared to tissue-specific progenitors. Direct interrogation of iron uptake demonstrated CSCs potently extract iron from the microenvironment more effectively than other tumor cells. Systematic interrogation of iron flux determined that CSCs preferentially require transferrin receptor and ferritin - two core iron regulators - to propagate and form tumors in vivo. Depleting ferritin disrupted CSC mitotic progression, through the STAT3-FoxM1 regulatory axis, revealing an iron-regulated CSC pathway. Iron is a unique, primordial metal fundamental for earliest life forms, and on which CSCs have an epigenetically programmed, targetable dependence.

2015-09-30 | GSE72203 | GEO

NCOA4-mediated ferritinophagy is a pancreatic cancer dependency via maintenance of iron bioavailability for iron-sulfur cluster proteins

Project description:Oncogenic KRAS rewires pancreatic ductal adenocarcinoma (PDAC) metabolism to promote dependence on autophagy and iron metabolism. NCOA4-mediated ferritinophagy links autophagy and iron metabolism as NCOA4 selectively targets ferritin, the cellular iron storage complex, via autophagy to the lysosome for ferritin degradation and release of iron for utilization. Using patient-derived and genetically engineered murine models of PDAC we now demonstrate that ferritinophagy is upregulated in PDAC to sustain iron availability thereby promoting PDAC progression. PDAC global quantitative proteomics reveals that ferritinophagy fuels iron-sulfur cluster synthesis to support mitochondrial homeostasis. Targeting NCOA4 leads to tumor growth delay and prolonged survival but with development of compensatory iron acquisition pathways. Finally, a ferritinophagy gain-of-function PDAC murine model demonstrates worse survival, and an elevated ferritinophagy expression signature predicts for worse overall survival in human PDAC patients. Together, our data define NCOA4-mediated ferritinophagy as a therapeutic target in PDAC and reveal that maintenance of cellular iron homeostasis is a critical cell autonomous function of PDAC autophagy.

2022-08-17 | PXD033356 | Pride

The Hyphal Associated Adhesin and Invasin Als3 of Candida albicans Mediates Iron Acquisition from Host Ferritin

Project description:Iron sequestration by host iron-binding proteins is an important mechanism of resistance to microbial infections. Inside oral epithelial cells, iron is stored within the ferritin, and is therefore usually not accessible to pathogenic microbes. We observed that the ferritin concentration within oral epithelial cells was directly related to their susceptibility to damage by the human pathogenic fungus Candida albicans. Thus, we hypothesized that host ferritin may be used as an iron source by this organism. A screen of C. albicans mutants lacking components of each of the three iron acquisition systems revealed that only the reductive pathway is involved in iron utilization from ferritin by this organism. Transcriptional profiling of wild-type and hyphal-defective C. albicans strains suggested that the C. albicans invasin-like protein Als3 plays a role in ferritin binding.

2008-05-20 | GSE11490 | GEO

Glial ferritin maintains self-renewal and proliferation of neural stem cells by supplying iron in Drosophila

Project description:Glial ferritin maintains self-renewal and proliferation of neural stem cells by supplying iron in Drosophila

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Masison2022 - Cellular ferritin iron storage

Project description:This is a small model of ferritin iron sequestration kinetics. The model’s parameter values were determined from published kinetic and binding experiments and the model was validated against independent data not used in its construction. Beyond its utility to investigate properties of ferritin iron sequestration itself, we propose this model to be used as a building block for larger models of iron metabolism in a variety of specific cell types.

2023-02-07 | MODEL2211030001 | BioModels

Epigenetic Profile in Preferential Iron Trafficking Characterizes Glioblastoma Stem-like Cells

2015-09-30 | GSE72201 | GEO

RNA-seq Profiles in Preferential Iron Trafficking Characterizes Glioblastoma Stem-like Cells

2015-09-30 | GSE72202 | GEO

Hierarchical maintenance of MLL myeloid leukemia stem cells

Project description:Hierarchical maintenance of MLL myeloid leukemia stem cells employs a transcriptional program shared with embryonic rather than adult stem cells The genetic programs that promote retention of self-renewing leukemia stem cells (LSCs) at the apex of cellular hierarchies in acute myeloid leukemia (AML) are not known. In a mouse model of human AML, LSCs exhibit variable frequencies that correlate with the initiating MLL oncogene and are maintained in a self-renewing state by a transcriptional sub-program more akin to that of embryonic stem cells (ESCs) than adult stem cells. The transcription/chromatin regulatory factors Myb, Hmgb3 and Cbx5 are critical components of the program and suffice for Hoxa/Meis-independent immortalization of myeloid progenitors when co-expressed, establishing the cooperative and essential role of an ESC-like LSC maintenance program ancillary to the leukemia initiating MLL/Hox/Meis program. Enriched expression of LSC maintenance and ESC-like program genes in normal myeloid progenitors and poor prognosis human malignancies links the frequency of aberrantly self-renewing progenitor-like cancer stem cells to prognosis in human cancer. This SuperSeries is composed of the SubSeries listed below.

2009-02-06 | GSE13796 | GEO

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