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Among all the organelles in an animal cell, only mitochondria have their own independent genomes. Animal mitochondrial DNA is a double-stranded, closed-circular molecule with around 20,000 base pairs. Mitochondrial DNA is unique in that one of its two strands, the heavy, or H, -strand is guanine rich, whereas the complementary strand is cytosine rich and called the light, or L, -strand. Compared to nuclear DNA, mitochondrial DNA has a very low percentage of non-coding regions and is marked by...
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Retroviruses are RNA viruses that have been shown to cause cancers in diverse species, including chickens, mice, cats, and monkeys. The RNA genomes of these viruses are first reverse-transcribed into single and then double-stranded DNA (dsDNA) copies. This dsDNA called proviral DNA then integrates into the host genome. Subsequently, the host cell transcribes the proviral DNA in concert with the chromosomal DNA. This leads to the production of viral RNA and proteins that assemble at the host...
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The present-day mitochondrial and chloroplast genomes have retained some of the characteristics of their ancestral prokaryotes and also have acquired new attributes during their evolution within eukaryotic cells. Like prokaryotic genomes, mitochondrial and chloroplast genomes neither bind with histone-like proteins nor show complex packaging into chromosome-like structures, as observed in eukaryotes. Unlike mitotic cell divisions observed in eukaryotic cells, mitochondria and chloroplasts...
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A reversible chemical reaction represents a chemical process that proceeds in both forward (left to right) and reverse (right to left) directions. When the rates of the forward and reverse reactions are equal, the concentrations of the reactant and product species remain constant over time and the system is at equilibrium. A special double arrow is used to emphasize the reversible nature of the reaction. The relative concentrations of reactants and products in equilibrium systems vary greatly;...
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Mitochondrial dynamics in cancer-induced cachexia.

Miranda van der Ende1, Sander Grefte2, Rogier Plas3

  • 1Division of Human Nutrition, Wageningen University and Research, Wageningen, Netherlands; Human and Animal Physiology, Wageningen University and Research, Wageningen, Netherlands.

Biochimica Et Biophysica Acta. Reviews on Cancer
|July 31, 2018
PubMed
Summary

Cancer cachexia involves severe muscle loss, impacting survival. This study reveals altered muscle mitochondrial gene expression in rodent models, highlighting new research avenues for this complex condition.

Keywords:
Animal modelsCancer-induced cachexiaMitochondriaMitochondrial dynamicsMuscle

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Area of Science:

  • Biochemistry
  • Molecular Biology
  • Oncology

Background:

  • Cancer-induced cachexia severely impacts patient quality of life, therapeutic outcomes, and survival rates.
  • This complex metabolic syndrome is characterized by significant muscle loss, with limited understanding of its pathophysiology and treatment options.
  • Emerging research suggests a critical role for muscle mitochondrial networks in cancer cachexia.

Purpose of the Study:

  • To address the lack of comprehensive data on muscle mitochondrial involvement in cancer cachexia.
  • To integrate and analyze gene and protein expression datasets from cancer-induced cachexia animal models.
  • To identify key molecular pathways and mechanisms underlying muscle wasting in cancer.

Main Methods:

  • Compiled a comprehensive database from 94 research papers detailing muscle protein or gene expression in cancer-induced cachexia.
  • Included data from 11 different rodent models of cancer cachexia.
  • Integrated four genome-wide transcriptome datasets from cancer-induced cachexia rodent models for in-depth analysis.

Main Results:

  • Identified decreased expression of genes associated with mitochondrial fusion, fission, ATP production, and mitochondrial density.
  • Observed increased expression of genes involved in reactive oxygen species (ROS) detoxification and mitophagy.
  • Highlighted significant alterations in mitochondrial dynamics and quality control pathways in cancer cachexia.

Conclusions:

  • Muscle mitochondrial dysfunction is a key feature of cancer-induced cachexia.
  • Mitochondrial dynamics, energy production, and quality control mechanisms are significantly perturbed.
  • Future research should investigate post-translational modifications of mitochondrial proteins to fully understand cancer cachexia.