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Related Concept Videos

Adaptive Mechanisms in Cancer Cells02:53

Adaptive Mechanisms in Cancer Cells

Cancer cells accumulate genetic changes at an abnormally rapid rate due to the defects in the DNA repair mechanisms. From an evolutionary perspective, such genetic instability is advantageous for cancer development. Mutant cell lines accumulate a series of beneficial mutations that contribute to their progression into cancer.
Some of the advantages that cancer cells have on normal cells include - enhanced ability to divide without terminally differentiating, induce new blood vessel formation,...
Cross-bridge Cycle01:26

Cross-bridge Cycle

As muscle contracts, the overlap between the thin and thick filaments increases, decreasing the length of the sarcomere—the contractile unit of the muscle—using energy in the form of ATP. At the molecular level, this is a cyclic, multistep process that involves binding and hydrolysis of ATP, and movement of actin by myosin.
Muscle Recovery and Fatigue01:24

Muscle Recovery and Fatigue

Muscle fatigue refers to the decline in a muscle's ability to maintain the force of contraction after prolonged activity. It primarily stems from changes within muscle fibers. Even before experiencing muscle fatigue, one may feel tired and have the urge to stop the activity. This response, known as central fatigue, occurs due to changes in the central nervous system, namely the brain and spinal cord. While there is no single mechanism that induces fatigue, it may serve as a protective response...
Electron Transport Chain: Complex I and II01:46

Electron Transport Chain: Complex I and II

The mitochondrial electron transport chain (ETC) is the main energy generation system in the eukaryotic cells. However, mitochondria also produce cytotoxic reactive oxygen species (ROS) due to the large electron flow during oxidative phosphorylation. While Complex I is one of the primary sources of superoxide radicals, ROS production by Complex II is uncommon and may only be observed in cancer cells with mutated complexes.
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Mitochondria01:37

Mitochondria

Mitochondria are eukaryotic cellular organelles that are known to produce energy through a process called oxidative phosphorylation. Besides their primary function, mitochondria are involved in various cellular processes, including cell growth, differentiation, signaling, metabolism, and senescence. Age-related changes cause a decline in mitochondrial quality and integrity due to increased mitochondrial mutations and oxidative damage. Thus, aging can severely impact mitochondrial functions,...
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Overview of Protein Metabolism

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Related Experiment Video

Updated: May 21, 2026

The Colon-26 Carcinoma Tumor-bearing Mouse as a Model for the Study of Cancer Cachexia
08:55

The Colon-26 Carcinoma Tumor-bearing Mouse as a Model for the Study of Cancer Cachexia

Published on: November 30, 2016

Cancer cachexia is associated with a decrease in skeletal muscle mitochondrial oxidative capacities without

Cloé M Julienne1, Jean-François Dumas, Caroline Goupille

  • 1INSERM U921, Nutrition, Croissance et Cancer, 37032, Tours, France.

Journal of Cachexia, Sarcopenia and Muscle
|June 1, 2012
PubMed
Summary

Cancer cachexia causes muscle wasting by reducing skeletal muscle mitochondrial oxidative capacity, specifically complex IV activity. This study found no change in ATP synthesis efficiency despite increased UCP2 gene expression.

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Evaluating the Role of Mitochondrial Function in Cancer-related Fatigue
08:56

Evaluating the Role of Mitochondrial Function in Cancer-related Fatigue

Published on: May 17, 2018

Related Experiment Videos

Last Updated: May 21, 2026

The Colon-26 Carcinoma Tumor-bearing Mouse as a Model for the Study of Cancer Cachexia
08:55

The Colon-26 Carcinoma Tumor-bearing Mouse as a Model for the Study of Cancer Cachexia

Published on: November 30, 2016

Evaluating the Role of Mitochondrial Function in Cancer-related Fatigue
08:56

Evaluating the Role of Mitochondrial Function in Cancer-related Fatigue

Published on: May 17, 2018

Area of Science:

  • Mitochondrial bioenergetics
  • Skeletal muscle physiology
  • Cancer cachexia research

Background:

  • Cancer cachexia is a wasting syndrome linked to negative energy balance.
  • Muscle mitochondrial dysfunction is implicated in cancer cachexia.
  • Understanding these mechanisms is crucial for therapeutic development.

Purpose of the Study:

  • To investigate skeletal muscle mitochondrial oxidative phosphorylation efficiency in a preclinical cancer cachexia model.
  • To analyze changes in muscle morphology, gene expression, and mitochondrial function.

Main Methods:

  • Utilized Berlin-Druckrey IX rats with peritoneal carcinosis (PC) as a cachexia model.
  • Assessed hindlimb muscle morphology, fiber type, and ubiquitin ligase/UCP gene expression.
  • Measured oxygen consumption and ATP synthesis rates in isolated muscle mitochondria.

Main Results:

  • PC rats exhibited significant muscle wasting, particularly in fast glycolytic fibers.
  • Increased MuRF1 and MAFbx gene expression observed in PC rat muscle.
  • Reduced State III and uncoupled respiration, with a 30% decrease in complex IV activity, were found in PC rat mitochondria.

Conclusions:

  • Skeletal muscle mitochondrial oxidative capacity is reduced in cancer cachexia due to impaired complex IV activity.
  • ATP synthesis efficiency remains unaltered, and no mitochondrial uncoupling occurs despite UCP2 overexpression.
  • These bioenergetic alterations may contribute to insulin resistance, lipid accumulation, and lactate production in cachexia.