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Iron Chelators Treatment on DMS-53 Human Lung Cancer Cell

ABSTRACT: 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. The DMS-53 cells were incubated with either control medium or this medium containing DFO (250 µM) or Dp44mT (25 µM) for 24 h at 37oC. These concentrations were used since our previous studies demonstrated that under these conditions these chelators lead to up-regulation of iron-responsive genes such as the TfR1 after this incubation time. Moreover, the higher concentration of DFO was implemented due to its limited ability to permeate cell membranes. Total RNA was isolated from cells in 1 mL of TRIzol® reagent (Invitrogen). Samples were then prepared and hybridized to the Human Genome U133 Plus 2.0 430 2.0. The human GeneChip® U133 Plus 2.0 consists of greater than 47,000 transcripts and variants from over 38,500 well characterized human genes. On completion of hybridization and washing, microarray chips were scanned with the Affymetrix GeneChip® Scanner 3000 (Affymetrix).

ORGANISM(S): Homo sapiens

SUBMITTER: Yu Yu

PROVIDER: S-ECPF-GEOD-26920 | biostudies-other |

REPOSITORIES: biostudies-other

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Iron Chelators Treatment on DMS-53 Human Lung Cancer Cell

2011-12-31 | GSE26920 | 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. The DMS-53 cells were incubated with either control medium or this medium containing DFO (250 µM) or Dp44mT (25 µM) for 24 h at 37oC. These concentrations were used since our previous studies demonstrated that under these conditions these chelators lead to up-regulation of iron-responsive genes such as the TfR1 after this incubation time. Moreover, the higher concentration of DFO was implemented due to its limited ability to permeate cell membranes. Total RNA was isolated from cells in 1 mL of TRIzol® reagent (Invitrogen). Samples were then prepared and hybridized to the Human Genome U133 Plus 2.0 430 2.0. The human GeneChip® U133 Plus 2.0 consists of greater than 47,000 transcripts and variants from over 38,500 well characterized human genes. On completion of hybridization and washing, microarray chips were scanned with the Affymetrix GeneChip® Scanner 3000 (Affymetrix).

2011-12-31 | E-GEOD-26920 | biostudies-arrayexpress

Iron Chelators Treatment on MCF-7 Human Breast Cancer Cell

Project description:Iron-deficiency affects 500 million people, yet 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-deficiency and the biological effects of iron chelators. We assessed the effect on whole genome gene expression of two iron chelators (desferrioxamine and 2-hydroxy-1-napthylaldehyde isonicotinoyl hydrazone) that have markedly different permeability properties. Sixteen genes were significantly regulated by both chelators, while a further 50 genes were regulated by either ligand. Most of the genes identified in this study have not been previously described to be iron-regulated and are important for understanding the molecular and cellular effects of iron-deficiency. The MCF-7 cells were incubated with either control medium or this medium containing DFO (250 µM) or 311 (25 µM) for 24 h at 37oC. These concentrations were used since our previous studies demonstrated that under these conditions these chelators lead to up-regulation of iron-responsive genes such as the TfR1 after this incubation time.8 Moreover, the higher concentration of DFO was implemented due to its limited ability to permeate cell membranes. Total RNA was isolated from cells in 1 mL of TRIzol® reagent (Invitrogen). Samples were then prepared and hybridized to the Human Genome U133 Plus 2.0 430 2.0. The human GeneChip® U133 Plus 2.0 consists of greater than 47,000 transcripts and variants from over 38,500 well characterized human genes. On completion of hybridization and washing, microarray chips were scanned with the Affymetrix GeneChip® Scanner 3000 (Affymetrix).

| S-ECPF-GEOD-17832 | biostudies-other

Iron Chelators Treatment on MCF-7 Human Breast Cancer Cell

2010-02-28 | GSE17832 | GEO

Iron Chelators Treatment on MCF-7 Human Breast Cancer Cell

Project description:Iron-deficiency affects 500 million people, yet 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-deficiency and the biological effects of iron chelators. We assessed the effect on whole genome gene expression of two iron chelators (desferrioxamine and 2-hydroxy-1-napthylaldehyde isonicotinoyl hydrazone) that have markedly different permeability properties. Sixteen genes were significantly regulated by both chelators, while a further 50 genes were regulated by either ligand. Most of the genes identified in this study have not been previously described to be iron-regulated and are important for understanding the molecular and cellular effects of iron-deficiency. The MCF-7 cells were incubated with either control medium or this medium containing DFO (250 ÂµM) or 311 (25 ÂµM) for 24 h at 37oC. These concentrations were used since our previous studies demonstrated that under these conditions these chelators lead to up-regulation of iron-responsive genes such as the TfR1 after this incubation time.8 Moreover, the higher concentration of DFO was implemented due to its limited ability to permeate cell membranes. Total RNA was isolated from cells in 1 mL of TRIzolÂ® reagent (Invitrogen). Samples were then prepared and hybridized to the Human Genome U133 Plus 2.0 430 2.0. The human GeneChipÂ® U133 Plus 2.0 consists of greater than 47,000 transcripts and variants from over 38,500 well characterized human genes. On completion of hybridization and washing, microarray chips were scanned with the Affymetrix GeneChipÂ® Scanner 3000 (Affymetrix).

2010-03-09 | E-GEOD-17832 | biostudies-arrayexpress

PM01183 on SCLC cell lines [ChIP-Seq, DMS-53]

Project description:detect the impact of lurbinectedin on transciption factor binding

2022-01-29 | GSE190520 | GEO

Human lung cancer cell lines DMS-273 (SCLC) and NCI-H1437 (NSCLC): scrambled vs. shRNA clones

Project description:Transcriptional profiling of two human lung cancer cell lines, DMS-273 (small cell lung cancer) and NCI-H1437 (non-small cell lung cancer), stably transfected either with innocuous scrambled shRNAs or SETDB1-specific.The objective was to identify global gene expression changes due to the depletion of the H3K9me3 methyltransferase SETDB1. 3 replicates for DMS-273 and 1 Control; 2 replicates for NCI-H1437 and 1 Control

| S-ECPF-GEOD-45175 | biostudies-other

Benefits of Iron Chelators in the Treatment of Parkinson's Disease.

Project description:As a novel discovered regulated cell death pattern, ferroptosis has been associated with the development of Parkinson's disease (PD) and has attracted widespread attention. Nevertheless, the relationship between ferroptosis and PD pathogenesis is still unclear. This study aims to investigate the effect of iron overload on dopaminergic (DA) neurons and its correlation with ferroptosis. Here we use nerve growth factor (NGF) induced PC12 cells which are derived from pheochromocytoma of the rat adrenal to establish a classical PD in vitro model. We found significantly decreased cell viability in NGF-PC12 cell under ammonium ferric citrate (FAC) administration. Moreover, excessive intracellular iron ions induced the increase of (reactive oxygen species) ROS release as well as the decrease of mitochondrial membrane potential in PC12-NGF cells. In addition, we also found that overloaded iron can activate cell apoptosis and ferroptosis pathways, which led to cell death. Furthermore, MPP-induced PD cells were characterized by mitochondrial shrinkage, decreased expression of glutathione peroxidase 4 (Gpx4) and ferritin heavy chain (FTH1), and increased divalent metal transporter (DMT1) and transferrin receptor 1 (TfR1) expression level. In contrast, Lip-1 and DFO increased the expression level of GPX4 and FTH1 compared to MPP-induced PD cell. In conclusion, we indicated that overloaded intracellular iron contributes to neurons death via apoptosis and ferroptosis pathways, while DFO, an iron chelator, can inhibit ferroptosis in order to protect the neurons in vitro.

| S-EPMC8053182 | biostudies-literature

Iron chelators target both proliferating and quiescent cancer cells.

Project description:Poorly vascularized areas of solid tumors contain quiescent cell populations that are resistant to cell cycle-active cancer drugs. The compound VLX600 was recently identified to target quiescent tumor cells and to inhibit mitochondrial respiration. We here performed gene expression analysis in order to characterize the cellular response to VLX600. The compound-specific signature of VLX600 revealed a striking similarity to signatures generated by compounds known to chelate iron. Validation experiments including addition of ferrous and ferric iron in excess, EXAFS measurements, and structure activity relationship analyses showed that VLX600 chelates iron and supported the hypothesis that the biological effects of this compound is due to iron chelation. Compounds that chelate iron possess anti-cancer activity, an effect largely attributed to inhibition of ribonucleotide reductase in proliferating cells. Here we show that iron chelators decrease mitochondrial energy production, an effect poorly tolerated by metabolically stressed tumor cells. These pleiotropic features make iron chelators an attractive option for the treatment of solid tumors containing heterogeneous populations of proliferating and quiescent cells.

| S-EPMC5141479 | biostudies-literature

Chelators in the treatment of iron accumulation in Parkinson's disease.

Project description:Iron is an essential element in the metabolism of all cells. Elevated levels of the metal have been found in the brains of patients of numerous neurodegenerative disorders, including Parkinson's disease (PD). The pathogenesis of PD is largely unknown, although it is thought through studies with experimental models that oxidative stress and dysfunction of brain iron homeostasis, usually a tightly regulated process, play significant roles in the death of dopaminergic neurons. Accumulation of iron is present at affected neurons and associated microglia in the substantia nigra of PD patients. This additional free-iron has the capacity to generate reactive oxygen species, promote the aggregation of ?-synuclein protein, and exacerbate or even cause neurodegeneration. There are various treatments aimed at reversing this pathologic increase in iron content, comprising both synthetic and natural iron chelators. These include established drugs, which have been used to treat other disorders related to iron accumulation. This paper will discuss how iron dysregulation occurs and the link between increased iron and oxidative stress in PD, including the mechanism by which these processes lead to cell death, before assessing the current pharmacotherapies aimed at restoring normal iron redox and new chelation strategies undergoing research.

| S-EPMC3382398 | biostudies-other

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