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Proteomic shift in mouse embryonic fibroblasts Pfa1 during L-Buthionine-sulfoximine (BSO) induced ferroptosis

ABSTRACT: This report provides data on ferroptosis induced proteomic response in immortalized mouse embryonic fibroblasts which are 4-OH-TAM-inducible Gpx4−/− (referred to as Pfa1 cells). Pfa1 cells are a valuable, widespread and well characterized model for ferroptosis research. We used L-Buthionine-sulfoximine (BSO) to induce ferroptosis and collected samples at 0h, 24h and 48 h after treatment. Untreated cells were used as a control. Pfa1 cells (kind gift from Marcus Conrad, Munich) were cultured in RPMI-1640 media (2 g/L glucose, 10% FBS, 2 mM Gibco GlutaMAX Supplement, 1% pen/strep) at 37C with 5% CO2 in a humidified incubator. Cells (300k) were seeded on Corning 100 mm tissue-culture treated culture dishes and incubated overnight. On the next day Pfa1 cells were treated with or without 30 µM BSO.

INSTRUMENT(S): Q Exactive HF-X

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Embryonic Fibroblast Cell Line, Fibroblast

SUBMITTER: Olga Kudryashova

LAB HEAD: Dr Dr Vsevolod V. Belousov

PROVIDER: PXD041415 | Pride | 2023-04-12

REPOSITORIES: Pride

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Proteomic shift in mouse embryonic fibroblasts Pfa1 during erastin-induced ferroptosis

Project description:This report provides data on ferroptosis induced proteomic response in immortalized mouse embryonic fibroblasts which are 4-OH-TAM-inducible Gpx4−/− (referred to as Pfa1 cells). Pfa1 cells are a valuable, widespread and well characterized model for ferroptosis research. In the first part of this batch, we used Erastin to induce ferroptosis and collected samples at 0h, 24h and 48h after treatment. Untreated cells were used as a control. In the second part, we tested Liproxtatin-1 ferroptosis inhibitor on Tamoxifen-induced Pfa1 cells after 0h, 24h, 48h. Tamoxifen-induced ferroptosis activation of these cells are in PRIDE PXD040094. Pfa1 cells (a kind gift from Marcus Conrad, Munich) were cultured in RPMI-1640 media (2 g/L glucose, 10% FBS, 2 mM Gibco GlutaMAX Supplement, 1% pen/strep) at 37C with 5% CO2 in a humidified incubator. Cells (300k) were seeded on Corning 100 mm tissue-culture treated culture dishes and incubated overnight. On the next day Pfa1 cells were treated with or without 0.5 µM erastin (E7781, Sigma-Aldrich). For experiment on ferroptosis inhibition Pfa1 cells were treated with or without 1 µM Tamoxifen and 0.5 µM Liproxtatin-1 simultaneously.

2023-07-11 | PXD041463 | Pride

Proteomic shift in mouse embryonic fibroblasts Pfa1 during ML210-induced ferroptosis

2023-07-10 | PXD041327 | Pride

Proteomic response on ferroptosis induction via GPX4 KO in mouse embryonic fibroblasts

Project description:In the present study, we report proteome data of mouse embryonic fibroblasts (MEF cells) and immortalized mouse embryonic fibroblasts which are 4-OH-TAM-inducible Gpx4−/− (Pfa1 cells). Ferroptosis in Pfa1 cells was induced with Tamoxifen (Tam) addition and three timepoints were collected: 0h, 24h and 48h. Wild-type MEF cells were also measured as an alternative control without Tam addition. Raw data for HEK293 cells are provided as an independent quality control. MEF and Pfa1 cells (both kind gift from Marcus Conrad, Munich) were cultured in RPMI-1640 media (2 g/L glucose, 10% FBS, 2 mM Gibco GlutaMAX Supplement, 1% pen/strep) at 37C with 5% CO2 in a humidified incubator. Cells (300k) were seeded on Corning 100 mm tissue-culture treated culture dishes and incubated overnight. On the next day Pfa1 cells were treated with or without 1 µM Tam.

2023-04-12 | PXD040094 | Pride

NINJ1 induces plasma membrane rupture and DAMP release during ferroptosis

Project description:Ferroptosis is a regulated form of necrotic cell death caused by an iron-dependent accumulation of oxidized phospholipids in cellular membranes, which culminates in plasma membrane rupture (PMR) and cell lysis. PMR is also a hallmark of other types of programmed necrosis, such as pyroptosis and necroptosis, where it is initiated by dedicated pore-forming cell death executors. Yet, whether ferroptosis-associated PMR is actively executed by a protein or driven by osmotic pressure remains unknown. Here, we investigated the role of ninjurin-1 (NINJ1), the recently identified executor of pyroptosis-associated PMR, in ferroptosis. We report that during ferroptosis NINJ1 oligomerizes and that Ninj1-deficiency protects macrophages and fibroblasts from ferroptosis-associated PMR. Mechanistically, we find that NINJ1 is dispensable for the early steps of ferroptosis, such as lipid peroxidation, channel-mediated calcium influx and cell swelling. By contrast, NINJ1 is required for early loss of plasma membrane integrity, an event that precedes complete PMR. Furthermore, NINJ1 mediates the release of cytosolic proteins and danger-associated molecular patterns (DAMPs) from ferroptotic cells, suggesting that targeting NINJ1 could be a therapeutic option to reduce ferroptosis-associated inflammation.

2024-02-15 | PXD047622 | Pride

Transferrin receptor is a specific ferroptosis marker

Project description:Ferroptosis is a form of regulated cell death driven by the iron-dependent accumulation of oxidized polyunsaturated-fatty-acid-containing phospholipids (PUFA-PLs). Three key molecular features of ferroptosis are peroxidation of PUFA-PLs, accumulation of redox-active ferrous iron, and defective lipid peroxide repair (Dixon and Stockwell, 2019). However, there is currently no reliable way to selectively stain ferroptotic cells in tissue sections to characterize the extent of ferroptosis in animal models of disease and in patient tissue samples. We sought to address this gap by immunizing mice with membranes from lymphoma cells treated with the ferroptosis inducer piperazine erastin (PE), and screening ~4,750 of the resulting monoclonal antibodies generated for their ability to selectively detect cells undergoing ferroptosis. We found that one antibody, termed 3F3 Ferroptotic Membrane Antibody (3F3-FMA), was effective as a selective ferroptosis-staining reagent using immunofluorescence (IF). The antigen of 3F3-FMA was identified by immunoprecipitation and mass spectrometry as the human transferrin receptor 1 protein (TfR1), which imports iron from the extracellular environment into cells. We validated this finding with several additional anti-TfR1 antibodies, and compared them to other potential ferroptosis-detecting reagents via immunofluorescence staining, using fluorescence microscopy and flow cytometry. We found that anti-TfR1 and anti-malondialdehyde (MDA) adduct antibodies were effective at reliably staining ferroptotic tumor cells in numerous cell culture and tissue contexts. In summary, these findings suggest that anti-TfR1 antibodies can be used to selectively label cells undergoing ferroptosis.

2020-03-10 | PXD017425 | Pride

mTOR Inhibition Suppresses Salinomycin-Induced Ferroptosis in Breast Cancer Stem Cells by Ironing Out Mitochondrial Dysfunctions

Project description:Ferroptosis constitutes a promising therapeutic strategy against cancer by efficiently targeting the highly tumorigenic and treatment-resistant cancer stem cells (CSCs). We previously showed that the lysosomal iron-targeting drug Salinomycin (Sal) was able to eliminate CSCs by triggering ferroptosis. Here, in a well-established breast CSCs model (human mammary epithelial HMLER CD24low/CD44high), we identified that pharmacological inhibition of mechanistic target of rapamycin (mTOR), suppresses Sal-induced ferroptosis. Mechanistically, mTOR inhibition modulates iron cellular flux and prevents the iron and ROS bursts induced by Sal. Besides, integration of multi-omics data identified mitochondria as a key target of Sal action. We demonstrated that mTOR inhibition prevents Sal-induced mitochondrial functional and structural alteration, and that Sal-induced metabolic plasticity is mainly dependent on the mTOR pathway. Overall, our findings provide experimental evidences on the detailed mechanisms of mTOR as a crucial effector of Sal-induced ferroptosis, and gives proof-of-concept that careful evaluation of such combination therapy (here mTOR and ferroptosis co-targeting) is required for effective treatment.

2023-12-20 | PXD041545 | Pride

Illumina Sequencing data of Insulator Proteins and the co-factor dMes-4

Project description:The Drosophila insulator-binding proteins (IBPs) dCTCF/Beaf32 mark the physical borders of chromosomal domains involving co-factors that participate in long-range interactions. Chromosomal borders are further enriched in specific histone modifications yet the implication of histone modifiers and nucleosome dynamics remains largely unknown in such context. Here, we show that IBP depletion impairs nucleosome dynamics over genes flanked by their binding sites. Biochemical purification identifies a key histone methyltransferase of H3K36, NSD/dMes-4, as a novel co-factor of IBPs involved in chromatin accessibility, which specifically co-regulates hundreds of genes flanked by Beaf32/dCTCF. dMes-4 presets chromatin before the recruitment of transcriptional activators including DREF that triggers Set2/Hypb-mediated H3K36me3, RNA splicing and nucleosome positioning. Our results unveil a model for how IBPs regulate gene expression and nucleosome dynamics through NSD/dMes-4, which may contribute to regulate H3K27me3 spreading. Together, our data suggest a division of labor for how IBPs may dynamically regulate chromatin organization depending on distinct co-factors. ChIP-Seq profiles of H3K36 methylation and RNA Pol II in Drosophila S2 cell line (wild-type) cells

2014-04-30 | E-GEOD-57165 | biostudies-arrayexpress

Phosphoproteomic analysis of Hemin- and Erastin-induced neuronal death

Project description:Analysis of the differences in phosphorylation in two ferroptosis subtypes (Hemin vs classical erastin-induced ferroptosis) in neurons, and sensitivity of these changes in phosphorylation levels to treatment with ferroptosis suppressor and MEK inhibitor U0126.

2022-01-28 | PXD029318 | Pride

RNA-seq of human pancreatic cancer cell line PANC-1 treated with RSL-3, N6F11, Fin56 and Erastin against untreated controls

Project description:Ferroptotic cell death is dependent on unrestricted lipid peroxidation rather than activation of apoptotic effector caspases. A large number of ferroptosis activators have been reported recently. We used gene sequencing to analyze the effects of four ferroptosis activators (RSL3, N6F11, Fin56 and Erastin) on global gene expression in human PDAC1 cell line.

2023-10-18 | E-MTAB-12241 | biostudies-arrayexpress

MNASE_seq_of_AGO2_Knock_Down_HeLaS3_cells

Project description:We knocked down AGO2 protein by RNAi in HeLaS3 human cell line. The current experiment aims at comparing nucleosome positioning in control and AGO2 knock down cells. HeLaS3 cell were cultured in DMEM. Cells were transfected with AGO2 siRNAs (or control siRNA) at day 1. On day 4 MNAse digestion of chromatin was performed. Mnase-digested chromatin DNA fragments were sequenced by paired-end DNA-seq.

2015-05-17 | E-MTAB-1844 | biostudies-arrayexpress

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