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Difference between revisions of "Schoepf 2020 Nat Commun"

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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, 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.
|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. https://doi.org/10.1038/s41467-020-15237-5
|info=[https://www.nature.com/articles/s41467-020-15237-5 Open Access] »[[File:O2k-brief.png|36px|link=https://wiki.oroboros.at/images/7/7d/Schoepf_2020_Nat_Commun_O2k-brief.pdf|O2k-brief]]
|info=Nat Commun 11:1487. [https://pubmed.ncbi.nlm.nih.gov/32198407/ PMID: 32198407 Open Access] »[[File:O2k-brief.png|36px|link=https://wiki.oroboros.at/images/7/7d/Schoepf_2020_Nat_Commun_O2k-brief.pdf|O2k-brief]]
|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
|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
|abstract=Rewiring of energy metabolism and adaptation of mitochondria are considered to impact on
|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
prostate cancer development and progression. Here we report on mitochondrial respiration,
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
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.
survival times.
|editor=[[Gnaiger E]],
|editor=[[Gnaiger E]],
|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«]]
== Cited by ==
::* 22 articles in PubMed (2021-12-27) https://pubmed.ncbi.nlm.nih.gov/32198407/
{{Template:Cited by Gnaiger 2021 MitoFit BCA}}
{{Template:Cited by Gnaiger 2020 BEC MitoPathways}}
{{Template:Cited by Gnaiger 2020 BEC MitoPhysiology}}
{{Labeling
{{Labeling
|area=Respiration, mtDNA;mt-genetics, mt-Medicine, Patients
|area=Respiration, mtDNA;mt-genetics, mt-Medicine, Patients
Line 33: Line 32:
|pathways=N, S, NS
|pathways=N, S, NS
|instruments=Oxygraph-2k
|instruments=Oxygraph-2k
|additional=Alert2020,
|additional=Alert2020, O2k-brief, BEC 2020.1, BEC 2020.2, MitoFit 2021 BCA
}}
}}
== 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«]]

Latest revision as of 15:11, 4 June 2022

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. https://doi.org/10.1038/s41467-020-15237-5

» Nat Commun 11:1487. PMID: 32198407 Open Access »O2k-brief

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

Cited by

Gnaiger E (2021) Bioenergetic cluster analysis – mitochondrial respiratory control in human fibroblasts. MitoFit Preprints 2021.8.


Gnaiger E (2021) Bioenergetic cluster analysis – mitochondrial respiratory control in human fibroblasts. MitoFit Preprints 2021.8. https://doi.org/10.26124/mitofit:2021-0008
Gnaiger 2020 BEC MitoPathways
Gnaiger E (2020) Mitochondrial pathways and respiratory control. An introduction to OXPHOS analysis. 5th ed. Bioenerg Commun 2020.2. https://doi.org/10.26124/bec:2020-0002


Gnaiger Erich et al ― MitoEAGLE Task Group (2020) Mitochondrial physiology. Bioenerg Commun 2020.1.
Gnaiger E et al ― MitoEAGLE Task Group (2020) Mitochondrial physiology. Bioenerg Commun 2020.1. doi:10.26124/bec:2020-0001.v1.



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 2020.1, BEC 2020.2, MitoFit 2021 BCA