Mitochondrial dynamics in cancer-induced cachexia

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8 Citations (Scopus)

Abstract

Cancer-induced cachexia has a negative impact on quality of life and adversely affects therapeutic outcomes and survival rates. It is characterized by, often severe, loss of muscle, with or without loss of fat mass. Insight in the pathophysiology of this complex metabolic syndrome and direct treatment options are still limited, which creates a research demand. Results from recent studies point towards a significant involvement of muscle mitochondrial networks. However, data are scattered and a comprehensive overview is lacking. This paper aims to fill existing knowledge gaps by integrating published data sets on muscle protein or gene expression from cancer-induced cachexia animal models. To this end, a database was compiled from 94 research papers, comprising 11 different rodent models. This was combined with four genome-wide transcriptome datasets of cancer-induced cachexia rodent models. Analysis showed that the expression of genes involved in mitochondrial fusion, fission, ATP production and mitochondrial density is decreased, while that of genes involved ROS detoxification and mitophagy is increased. Our results underline the relevance of including post-translational modifications of key proteins involved in mitochondrial functioning in future studies on cancer-induced cachexia.

Original languageEnglish
Pages (from-to)137-150
JournalBiochimica et Biophysica Acta - Reviews on Cancer
Volume1870
Issue number2
DOIs
Publication statusPublished - 1 Dec 2018

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Mitochondrial Dynamics
Cachexia
Rodentia
Neoplasms
Mitochondrial Degradation
Gene Expression
Muscles
Muscle Proteins
Post Translational Protein Processing
Transcriptome
Research
Survival Rate
Animal Models
Adenosine Triphosphate
Fats
Quality of Life
Genome
Databases
Therapeutics
Genes

Keywords

  • Animal models
  • Cancer-induced cachexia
  • Mitochondria
  • Mitochondrial dynamics
  • Muscle

Cite this

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title = "Mitochondrial dynamics in cancer-induced cachexia",
abstract = "Cancer-induced cachexia has a negative impact on quality of life and adversely affects therapeutic outcomes and survival rates. It is characterized by, often severe, loss of muscle, with or without loss of fat mass. Insight in the pathophysiology of this complex metabolic syndrome and direct treatment options are still limited, which creates a research demand. Results from recent studies point towards a significant involvement of muscle mitochondrial networks. However, data are scattered and a comprehensive overview is lacking. This paper aims to fill existing knowledge gaps by integrating published data sets on muscle protein or gene expression from cancer-induced cachexia animal models. To this end, a database was compiled from 94 research papers, comprising 11 different rodent models. This was combined with four genome-wide transcriptome datasets of cancer-induced cachexia rodent models. Analysis showed that the expression of genes involved in mitochondrial fusion, fission, ATP production and mitochondrial density is decreased, while that of genes involved ROS detoxification and mitophagy is increased. Our results underline the relevance of including post-translational modifications of key proteins involved in mitochondrial functioning in future studies on cancer-induced cachexia.",
keywords = "Animal models, Cancer-induced cachexia, Mitochondria, Mitochondrial dynamics, Muscle",
author = "{van der Ende}, Miranda and Sander Grefte and Rogier Plas and Jocelijn Meijerink and Witkamp, {Renger F.} and Jaap Keijer and {van Norren}, Klaske",
year = "2018",
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T1 - Mitochondrial dynamics in cancer-induced cachexia

AU - van der Ende, Miranda

AU - Grefte, Sander

AU - Plas, Rogier

AU - Meijerink, Jocelijn

AU - Witkamp, Renger F.

AU - Keijer, Jaap

AU - van Norren, Klaske

PY - 2018/12/1

Y1 - 2018/12/1

N2 - Cancer-induced cachexia has a negative impact on quality of life and adversely affects therapeutic outcomes and survival rates. It is characterized by, often severe, loss of muscle, with or without loss of fat mass. Insight in the pathophysiology of this complex metabolic syndrome and direct treatment options are still limited, which creates a research demand. Results from recent studies point towards a significant involvement of muscle mitochondrial networks. However, data are scattered and a comprehensive overview is lacking. This paper aims to fill existing knowledge gaps by integrating published data sets on muscle protein or gene expression from cancer-induced cachexia animal models. To this end, a database was compiled from 94 research papers, comprising 11 different rodent models. This was combined with four genome-wide transcriptome datasets of cancer-induced cachexia rodent models. Analysis showed that the expression of genes involved in mitochondrial fusion, fission, ATP production and mitochondrial density is decreased, while that of genes involved ROS detoxification and mitophagy is increased. Our results underline the relevance of including post-translational modifications of key proteins involved in mitochondrial functioning in future studies on cancer-induced cachexia.

AB - Cancer-induced cachexia has a negative impact on quality of life and adversely affects therapeutic outcomes and survival rates. It is characterized by, often severe, loss of muscle, with or without loss of fat mass. Insight in the pathophysiology of this complex metabolic syndrome and direct treatment options are still limited, which creates a research demand. Results from recent studies point towards a significant involvement of muscle mitochondrial networks. However, data are scattered and a comprehensive overview is lacking. This paper aims to fill existing knowledge gaps by integrating published data sets on muscle protein or gene expression from cancer-induced cachexia animal models. To this end, a database was compiled from 94 research papers, comprising 11 different rodent models. This was combined with four genome-wide transcriptome datasets of cancer-induced cachexia rodent models. Analysis showed that the expression of genes involved in mitochondrial fusion, fission, ATP production and mitochondrial density is decreased, while that of genes involved ROS detoxification and mitophagy is increased. Our results underline the relevance of including post-translational modifications of key proteins involved in mitochondrial functioning in future studies on cancer-induced cachexia.

KW - Animal models

KW - Cancer-induced cachexia

KW - Mitochondria

KW - Mitochondrial dynamics

KW - Muscle

U2 - 10.1016/j.bbcan.2018.07.008

DO - 10.1016/j.bbcan.2018.07.008

M3 - Review article

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JO - Biochimica et Biophysica Acta - Reviews on Cancer

JF - Biochimica et Biophysica Acta - Reviews on Cancer

SN - 0304-419X

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