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Schoepf 2019 MitoFit Preprint Arch

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Gnaiger 2019 MitoFit Preprints
       
Gnaiger MitoFit Preprints 2020.4
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Schoepf 2019 MitoFit Preprint Arch

Publications in the MiPMap
Schöpf B, Weissensteiner H, Schäfer G, Fazzini F, Charoentong P, Naschberger A, Rupp B, Fendt L, Bukur V, Eichelbrönner 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. https://doi.org/10.26124/mitofit:190003 - 2020-03-20 published in »Nature Communications 11:1487«

» MitoFit Preprint Arch 2019.3.

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OXPHOS remodeling in high-grade prostate cancer involves mtDNA mutations and a prognostic gene expression signature


MitoFit Prep 2019.3. (2019) MitoFit Prep

Abstract: Version 1 (v1) 2019-06-11 doi:10.26124/mitofit:190003 - 2020-03-20 Published in »Nature Communications 11:1487«

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. Keywords: Mitochondria, high-resolution respirometry, oxidative phosphorylation, mitochondrial DNA mutation, mtDNA heteroplasmy, metabolic reprograming Bioblast editor: Gnaiger E

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