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mice, pancreatic, pubmed, fig, gpx, article, cell, cancer, google, scholar, depletion, ferroptosis, cas, pdac, highiron, tmem, tumor, diet, supplementary, expression, dna, pancreas, ohg, test, central, damage, tumorigenesis, death, macrophages, data, nature, macrophage, kcg, cells, krasdriven, micegroup, activation, analysis, oxidative, months, multiple, pancreatitis, anova, tukeys, comparisons, pathway, twoway, iron, control, rridab,

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nature portfolio csf2/granulocyte/macrophage colony-stimulating factor57 china-japan union hospital privacy policy research design log-rank [mantel–cox] test phosphate-buffered saline media advertising cn/index tmem173-dependent dna-sensing pathway gas chromatography-mass spectrometry sided log-rank test reprints l-arginine-induced pancreatitis developing nature 532 nature 569 nature 520 nature 553 nature bone marrow-derived macrophages kras-driven animal death high-iron diet-induced 4-hne mediating kras-driven tumorigenesis kras-driven pancreatic tumorigenesis light–dark diurnal cycle laser-scanning confocal microscope author information authors kras-driven mouse model pre-invasive precursor lesion elisa kits mitochondrial iron-mediated immunometabolism 8-ohg-induced cell migration 8-ohg-induced macrophage migration kras-mediated panin formation social media mincle-induced immune suppression ras mutation-independent pathways8 stroma-derived mrna signal oxidatively-induced dna damage gpx4 depletion-dependent tumorigenesis kras-mutant pancreatic carcinogenesis l-arginine-induced pancreatitis promote kras-driven pdac cre-inducible conditional allele selected-reaction monitoring mode 8-ohg-tmem173 pathway contributes telomere signal-free end administered anti-8-ohg antibodies anti-8-ohg antibody treatment metastasis suppressor n-myc

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         description:Ferroptosis is a more recently recognized form of cell death that relies on iron-mediated oxidative damage. Here, we evaluate the impact of high-iron diets or depletion of Gpx4, an antioxidant enzyme reported as an important ferroptosis suppressor, in the pancreas of mice with cerulean- or L-arginine-induced pancreatitis, and in an oncogenic Kras murine model of spontaneous pancreatic ductal adenocarcinoma (PDAC). We find that either high-iron diets or Gpx4 depletion promotes 8-OHG release and thus activates the TMEM173/STING-dependent DNA sensor pathway, which results in macrophage infiltration and activation during Kras-driven PDAC in mice. Consequently, the administration of liproxstatin-1 (a ferroptosis inhibitor), clophosome-mediated macrophage depletion, or pharmacological and genetic inhibition of the 8-OHG-TMEM173 pathway suppresses Kras-driven pancreatic tumorigenesis in mice. GPX4 is also a prognostic marker in patients with PDAC. These findings provide pathological and mechanistic insights into ferroptotic damage in PDAC tumorigenesis in mice. Ferroptosis is an iron-dependent mechanism of cell death. In this mouse study, the authors show that diets high in iron or depletion of the antioxidant Gpx4 potentiates pancreatic damage and tumour formation by activating the DNA damage pathway and recruiting macrophages to the pancreas.
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      headline:Ferroptotic damage promotes pancreatic tumorigenesis through a TMEM173/STING-dependent DNA sensor pathway
      description:Ferroptosis is a more recently recognized form of cell death that relies on iron-mediated oxidative damage. Here, we evaluate the impact of high-iron diets or depletion of Gpx4, an antioxidant enzyme reported as an important ferroptosis suppressor, in the pancreas of mice with cerulean- or L-arginine-induced pancreatitis, and in an oncogenic Kras murine model of spontaneous pancreatic ductal adenocarcinoma (PDAC). We find that either high-iron diets or Gpx4 depletion promotes 8-OHG release and thus activates the TMEM173/STING-dependent DNA sensor pathway, which results in macrophage infiltration and activation during Kras-driven PDAC in mice. Consequently, the administration of liproxstatin-1 (a ferroptosis inhibitor), clophosome-mediated macrophage depletion, or pharmacological and genetic inhibition of the 8-OHG-TMEM173 pathway suppresses Kras-driven pancreatic tumorigenesis in mice. GPX4 is also a prognostic marker in patients with PDAC. These findings provide pathological and mechanistic insights into ferroptotic damage in PDAC tumorigenesis in mice. Ferroptosis is an iron-dependent mechanism of cell death. In this mouse study, the authors show that diets high in iron or depletion of the antioxidant Gpx4 potentiates pancreatic damage and tumour formation by activating the DNA damage pathway and recruiting macrophages to the pancreas.
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