IP-MS data for identifying potential ferroptosis-associated and ISG15-related transcription factors
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo Sapiens
SUBMITTER: 
Jiayi Wang
PROVIDER: PXD072900 | iProX | Fri Jan 09 00:00:00 GMT 2026
REPOSITORIES: iProX
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Project description:Erastin is a small molecular compound which inhibits the system Xc- and prevents the import of cystine, reducing glutathione (GSH) biosynthesis and glutathione peroxidase 4 (GPX4) activity, and finally inducing cell death via ferroptosis. To establish a model of Erastin induced ferroptosis in glioma cells, U87 cells were treated of Erastin (10 μM, 72 h). Combination analysis of HiChIP, ChIP-seq and RNA-seq data suggests that change of chromatin loops mediated by 3D chromatin structure regulate gene expressions in glioma ferroptosis. Genes that regulated by 3D chromatin structure include genes that were reported function in ferroptosis like MDM2 and TXRND1. We propose a new regulatory mechanism governing glioma cell ferroptosis by 3D chromatin structure.
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Project description:To seek ferroptosis related genes in liver cancer cells, we treated HepG2 cells using ferroptosis inducer Erastin and inhibitor Ferrostatin, respectively. We found that a subset of genes were up-regulated in Erastin treatment groups and down-regulated in Ferrostatin treatment groups, suggesting that these genes might be correlated with ferroptosis.
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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.
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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.
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Project description:The coordinated and sequential interactions between drug-loaded nanocarriers and key genes within the cellular ferroptosis pathway are crucial for maintaining the survival and functional stability of PC12 neuronal cells. In this report, we demonstrate that quercetin-loaded PQR NPs serve as a key regulatory vehicle in counteracting Erastin-induced damage to PC12 cells. The absence of PQR NPs markedly heightens PC12 cells' susceptibility to Erastin-induced ferroptosis, a phenomenon reversible through exogenous administration of PQR NPs. Furthermore, PQR NPs interact both physically and functionally with core ferroptosis pathway genes (such as GPX4) and epigenetic modifiers, thereby regulating the expression levels of ferroptosis-related genes during Erastin-induced injury. Although PQR NPs are not essential for the transcriptional activity of core genes themselves, the quercetin delivery and release process mediated by PQR NPs is indispensable for scavenging excess reactive oxygen species within cells, maintaining GPX4 expression stability, and inhibiting Erastin-induced lipid peroxidation. Collectively, our data provide a molecular framework for how nanodelivery systems exert cytoprotective effects by regulating ferroptosis pathway gene expression. In this process, PQR NPs deliver quercetin and modulate the expression balance of key ferroptosis genes, thereby counteracting Erastin-induced damage in PC12 cells.
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