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Difference between revisions of "Schoepf 2020 Nat Commun"

From Bioblast
(Created page with "{{Publication |title=Schöpf Bernd, Weissensteiner Hansi, Schäfer Georg, Fazzini Federica, Charoentong Pornpimol, Naschberger Andreas, Rupp Bernhard, Fendt Liane, Bukur Vales...")
 
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{{Publication
{{Publication
|title=Schöpf Bernd, Weissensteiner Hansi, Schäfer Georg, Fazzini Federica, Charoentong Pornpimol, Naschberger Andreas, Rupp Bernhard, Fendt Liane, Bukur Valesca, Giese Irina, Patrick Sorn, Sant’Anna-Silva Ana Carolina, Iglesias-Gonzalez Javier, Sahin Ugur, Kronenberg Florian, Gnaiger Erich, Klocker Helmut (2020) OXPHOS remodeling in high-grade prostate cancer involves mtDNA mutations and increased succinate oxidation. Nat Commun 2020-03-20 [Epub ahead of print].
|title=Schöpf Bernd, Weissensteiner Hansi, Schäfer Georg, Fazzini Federica, Charoentong Pornpimol, Naschberger Andreas, Rupp Bernhard, Fendt Liane, Bukur Valesca, Giese Irina, Sorn Patrick, Sant’Anna-Silva Ana Carolina, Iglesias-Gonzalez Javier, Sahin Ugur, Kronenberg Florian, Gnaiger Erich, Klocker Helmut (2020) OXPHOS remodeling in high-grade prostate cancer involves mtDNA mutations and increased succinate oxidation. Nat Commun 2020-03-20 [Epub ahead of print].
|authors=Schoepf Bernd, Weissensteiner Hansi, Schaefer Georg, Fazzini Federica, Charoentong Pornpimol, Naschberger Andreas, Rupp Bernhard, Fendt Liane, Bukur Valesca, Giese Irina, Patrick Sorn, Sant’Anna-Silva Ana Carolina, Iglesias-Gonzalez Javier, Sahin Ugur, Kronenberg Florian, Gnaiger Erich, Klocker Helmut
|authors=Schoepf Bernd, Weissensteiner Hansi, Schaefer Georg, Fazzini Federica, Charoentong Pornpimol, Naschberger Andreas, Rupp Bernhard, Fendt Liane, Bukur Valesca, Giese Irina, Sorn Patrick, Sant’Anna-Silva Ana Carolina, Iglesias-Gonzalez Javier, Sahin Ugur, Kronenberg Florian, Gnaiger Erich, Klocker Helmut
|year=2020
|year=2020
|journal=Nat Commun
|journal=Nat Commun
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|mipnetlab=AT Innsbruck Gnaiger E, AT Innsbruck Oroboros
|mipnetlab=AT Innsbruck Gnaiger E, AT Innsbruck Oroboros
}}
}}
== MitoFit Preprint ==
::::* Schöpf et al (2019) OXPHOS remodeling in high-grade prostate cancer involves mtDNA mutations and a prognostic gene expression signature. MitoFit Preprint Arch [[doi:10.26124/mitofit:190003]]. - [[Schoepf 2019 MitoFit Preprint Arch |»Bioblast link«]]
{{Labeling
{{Labeling
|area=Respiration, mtDNA;mt-genetics, mt-Medicine, Patients
|area=Respiration, mtDNA;mt-genetics, mt-Medicine, Patients

Revision as of 14:46, 18 March 2020

Publications in the MiPMap
Schöpf Bernd, Weissensteiner Hansi, Schäfer Georg, Fazzini Federica, Charoentong Pornpimol, Naschberger Andreas, Rupp Bernhard, Fendt Liane, Bukur Valesca, Giese Irina, Sorn Patrick, Sant’Anna-Silva Ana Carolina, Iglesias-Gonzalez Javier, Sahin Ugur, Kronenberg Florian, Gnaiger Erich, Klocker Helmut (2020) OXPHOS remodeling in high-grade prostate cancer involves mtDNA mutations and increased succinate oxidation. Nat Commun 2020-03-20 [Epub ahead of print].


Schoepf Bernd, Weissensteiner Hansi, Schaefer Georg, Fazzini Federica, Charoentong Pornpimol, Naschberger Andreas, Rupp Bernhard, Fendt Liane, Bukur Valesca, Giese Irina, Sorn Patrick, Sant’Anna-Silva Ana Carolina, Iglesias-Gonzalez Javier, Sahin Ugur, Kronenberg Florian, Gnaiger Erich, Klocker Helmut (2020) Nat Commun

Abstract: Rewiring of energy metabolism and adaptation of mitochondria are considered to impact on prostate cancer development and progression. Here we report on mitochondrial respiration, DNA mutations and gene expression in paired benign/malignant human prostate tissue samples. Results reveal reduced respiratory capacities with NADH-pathway substrates glutamate and malate in malignant tissue and a significant metabolic shift towards higher succinate oxidation, particularly in high-grade tumors. The load of potentially deleterious mitochondrial-DNA mutations is higher in tumors and associated with unfavorable risk factors. High levels of potentially deleterious mutations in mitochondrial Complex I-encoding genes are associated with a 70% reduction in NADH-pathway capacity and compensation by increased succinate-pathway capacity. Structural analyses of these mutations reveal amino acid alterations leading to potentially deleterious effects on Complex I, supporting a causal relationship. A metagene signature extracted from the transcriptome of tumor samples exhibiting a severe mitochondrial phenotype enables identification of tumors with shorter survival times.

Bioblast editor: Gnaiger E O2k-Network Lab: AT Innsbruck Gnaiger E, AT Innsbruck Oroboros

MitoFit Preprint


Labels: MiParea: Respiration, mtDNA;mt-genetics, mt-Medicine, Patients  Pathology: Cancer 

Organism: Human  Tissue;cell: Genital, Other cell lines  Preparation: Permeabilized cells, Permeabilized tissue  Enzyme: Complex I  Regulation: Coupling efficiency;uncoupling, Flux control, Inhibitor  Coupling state: LEAK, ROUTINE, OXPHOS, ET  Pathway: N, S, NS  HRR: Oxygraph-2k 

Alert2020