Schoepf 2019 MitoFit Preprint Arch: Difference between revisions
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|authors=Schoepf | |authors=Schoepf Bernd, Weissensteiner H, Schaefer G, Fazzini F, Charoentong P, Naschberger A, Rupp B, Fendt Liane, Bukur V, Eichelbroenner I, Sorn P, Sahin U, Kronenberg F, Gnaiger Erich, Klocker Helmut | ||
|year=2019 | |year=2019 | ||
|journal=MitoFit Preprint Arch | |journal=MitoFit Preprint Arch | ||
|abstract=''' | |abstract='''2020-02-25 Accepted for publication in ''NATURE Communications''.''' | ||
Version 1 ('''v1''') '''2019-06-11''' [http://www.mitofit.org/images/d/dc/Schoepf_2019_MitoFit_Preprint_Arch.pdf doi:10.26124/mitofit:190003] | Version 1 ('''v1''') '''2019-06-11''' [http://www.mitofit.org/images/d/dc/Schoepf_2019_MitoFit_Preprint_Arch.pdf doi:10.26124/mitofit:190003] |
Revision as of 13:53, 25 February 2020
Schoepf 2019 MitoFit Preprint Arch
SchΓΆpf B, Weissensteiner H, SchΓ€fer G, Fazzini F, Charoentong P, Naschberger A, Rupp B, Fendt L, Bukur V, EichelbrΓΆnner I, Sorn P, Sahin U, Kronenberg F, Gnaiger E, Klocker H (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. |
Β»
Schoepf Bernd, Weissensteiner H, Schaefer G, Fazzini F, Charoentong P, Naschberger A, Rupp B, Fendt Liane, Bukur V, Eichelbroenner I, Sorn P, Sahin U, Kronenberg F, Gnaiger Erich, Klocker Helmut (2019) MitoFit Preprint Arch
Abstract: 2020-02-25 Accepted for publication in NATURE Communications.
Version 1 (v1) 2019-06-11 doi:10.26124/mitofit:190003
Rewiring of energy metabolism and adaptation of mitochondrial respiratory functions are considered to impact on prostate cancer development and progression. High-resolution respirometry of paired benign and malignant human prostate tissue samples revealed reduced respiratory capacities with NADH-pathway substrates glutamate and malate in malignant tissue and a significant metabolic shift towards respiratory capacity with succinate, particularly in high-grade tumors. The load of potentially deleterious mitochondrial-DNA mutations was higher in tumor tissue and associated with unfavorable risk factors. High levels of potentially deleterious mutations in mitochondrial Complex I-encoding genes were associated with a 70% reduction in NADH-pathway capacity and compensation by increased S-pathway capacity. Structural analyses of these mutations revealed amino acid alterations leading to potentially deleterious effects on Complex I, supporting a causal relationship. RNA-seq revealed a signature of metabolic enzymes corresponding to the altered mitochondrial respiratory pathways and enabled extraction of a metagene set for prediction of shorter disease-free survival. β’ Keywords: Mitochondria, high-resolution respirometry, oxidative phosphorylation, mitochondrial DNA mutation, mtDNA heteroplasmy, metabolic reprograming β’ Bioblast editor: Gnaiger E β’ O2k-Network Lab: AT Innsbruck Oroboros, AT Innsbruck Gnaiger E
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Preprints for Gentle Science
Β» MitoFit Preprints - the Open Access preprint server for mitochondrial physiology and bioenergetics
Labels: MiParea: Respiration, mtDNA;mt-genetics, nDNA;cell genetics, mt-Medicine
Pathology: Cancer
Stress:Oxidative stress;RONS
Organism: Human
Tissue;cell: Genital
Preparation: Permeabilized tissue
Enzyme: Complex I, TCA cycle and matrix dehydrogenases
Coupling state: LEAK, OXPHOS, ET Pathway: F, N, S, NS, ROX HRR: Oxygraph-2k
MitoEAGLEPublication