Schoepf 2020 Nat Commun: Difference between revisions
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::::* 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«]] | ::::* 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«]] | ||
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|area=Respiration, mtDNA;mt-genetics, mt-Medicine, Patients | |area=Respiration, mtDNA;mt-genetics, mt-Medicine, Patients |
Revision as of 11:14, 16 January 2021
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 11:1487. |
» Open Access »
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
- 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. - »Bioblast link«
Cited by
Template:Cited by Gnaiger 2000 BEC MitoPathways
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, O2k-brief, BEC 2020.2