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Difference between revisions of "Schoepf 2016 Abstract Mito Xmas Meeting Innsbruck"

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{{Abstract
{{Abstract
|title=
|title=Mitochondrial Function in Primary Prostate Cancer.
|authors=
 
|authors=Schöpf B, Weissensteiner H, Charoentong P, Schäfer G, Bukur V, Fendt L, Trajanoski Z, Kronenberg F, Gnaiger E & Klocker H
|year=2016
|year=2016
|event=Mito Xmas Meeting 2016 Innsbruck AT
|event=Mito Xmas Meeting 2016 Innsbruck AT
|abstract=
|abstract=Reprogramming of energy metabolism is a hallmark of cancer. Mutations in the mitochondrial DNA (mtDNA) might contribute to cancer development and progression. We analyzed mitochondrial respiration of fresh malignant and non-malignant prostate tissue samples obtained from 50 prostate cancer patients via High-Resolution Respirometry (HRR), determined mtDNA copy numbers by duplex qPCR, sequenced the whole mtDNAs using Next-Generation Sequencing (NGS) and analyzed expression of mitochondria-related genes in a subset of 16 cases by RNA-sequencing. HRR uncovered a shift of respiratory activity from mitochondrial complex I to complex II accompanied by a substrate shift toward higher respiratory activity elicited especially by succinate and pyruvate. The mutation load was significantly higher in tumor tissue compared to the non-malignant counterpart. Heteroplasmy levels of potentially deleterious mutations in mtDNA genes correlated significantly with reduced complex I respiration capacity. RNA-seq revealed a signature of differentially expressed metabolic enzymes in tumors exhibiting a severe compared to a mild complex CI mt-phenotype. The gene signature corresponded to observed altered substrates effects on respiration, e.g. increased pyruvate and citrate and decreased glutamate oxidation.
 
 


|mipnetlab=AT Innsbruck MitoFit, AT Innsbruck SBI
}}
}}
{{Labeling
{{Labeling
|event=Poster
}}
}}
== Affiliations ==
== Affiliations ==


::::  
:::: Schöpf B(1), Weissensteiner H(1), Charoentong P(2), Schäfer G(3,4), Bukur V(5), Fendt L(1), Trajanoski Z(2), Kronenberg F(1), Gnaiger E(6) & Klocker H(3)


::::#
::::# Div Genetic Epidemiology, Dept Medical Genetics, Molecular Clinical Pharmacology
::::# Div Bioinformatics, Biocenter
::::# Div Experimental Urology, Dept Urology
::::# Dept Pathology
::::# TRON gGmbH-Translational Oncology, Johannes-Gutenberg-University Medical Center, Mainz, Germany
::::# Dept General Transplant Surgery, D. Swarovski Research Laboratory, Medical Univ Innsbruck, Austria.

Revision as of 14:59, 7 December 2016

Mitochondrial Function in Primary Prostate Cancer.

Link:

Schöpf B, Weissensteiner H, Charoentong P, Schäfer G, Bukur V, Fendt L, Trajanoski Z, Kronenberg F, Gnaiger E & Klocker H (2016)

Event: Mito Xmas Meeting 2016 Innsbruck AT

Reprogramming of energy metabolism is a hallmark of cancer. Mutations in the mitochondrial DNA (mtDNA) might contribute to cancer development and progression. We analyzed mitochondrial respiration of fresh malignant and non-malignant prostate tissue samples obtained from 50 prostate cancer patients via High-Resolution Respirometry (HRR), determined mtDNA copy numbers by duplex qPCR, sequenced the whole mtDNAs using Next-Generation Sequencing (NGS) and analyzed expression of mitochondria-related genes in a subset of 16 cases by RNA-sequencing. HRR uncovered a shift of respiratory activity from mitochondrial complex I to complex II accompanied by a substrate shift toward higher respiratory activity elicited especially by succinate and pyruvate. The mutation load was significantly higher in tumor tissue compared to the non-malignant counterpart. Heteroplasmy levels of potentially deleterious mutations in mtDNA genes correlated significantly with reduced complex I respiration capacity. RNA-seq revealed a signature of differentially expressed metabolic enzymes in tumors exhibiting a severe compared to a mild complex CI mt-phenotype. The gene signature corresponded to observed altered substrates effects on respiration, e.g. increased pyruvate and citrate and decreased glutamate oxidation.


O2k-Network Lab: AT Innsbruck MitoFit, AT Innsbruck SBI


Labels:






Event: Poster 


Affiliations

Schöpf B(1), Weissensteiner H(1), Charoentong P(2), Schäfer G(3,4), Bukur V(5), Fendt L(1), Trajanoski Z(2), Kronenberg F(1), Gnaiger E(6) & Klocker H(3)
  1. Div Genetic Epidemiology, Dept Medical Genetics, Molecular Clinical Pharmacology
  2. Div Bioinformatics, Biocenter
  3. Div Experimental Urology, Dept Urology
  4. Dept Pathology
  5. TRON gGmbH-Translational Oncology, Johannes-Gutenberg-University Medical Center, Mainz, Germany
  6. Dept General Transplant Surgery, D. Swarovski Research Laboratory, Medical Univ Innsbruck, Austria.