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Related Concept Videos

Cancer Prevention02:59

Cancer Prevention

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Several factors can increase the risk of cancer in an individual. About 50% of cancer cases can be prevented by adopting a healthy lifestyle, regular exercise, eating healthy, and following a modest cancer prevention diet. Epidemiological studies have consistently shown that populations with vegetable and fruit-rich diets have reduced the incidence of cancer. On the other hand, populations who have a diet rich in animal fat, red meat, junk food, or high calories are predisposed to cancer.
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Electron Transport Chain: Complex I and II01:46

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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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Adaptive Mechanisms in Cancer Cells02:53

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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.
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The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
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Exercise and Cardiovascular Response01:20

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Exercise significantly impacts cardiovascular response, which is crucial for understanding patient health and designing effective treatment plans.
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Exercise and Muscle Performance01:27

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Exercise induces a range of adaptations in muscle tissue, depending on the type and duration of activity. Such physical training can be broadly categorized into two types: endurance exercises and resistance exercises.
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Related Experiment Video

Updated: Dec 21, 2025

Improving Strength, Power, Muscle Aerobic Capacity, and Glucose Tolerance through Short-term Progressive Strength Training Among Elderly People
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Exercise training reverses cancer-induced oxidative stress and decrease in muscle COPS2/TRIP15/ALIEN.

Christiano R R Alves1, Willian das Neves2, Ney R de Almeida3

  • 1School of Physical Education and Sport, University of Sao Paulo, Sao Paulo, Brazil; Section on Integrative Physiology and Metabolism, Joslin Diabetes Center, Harvard Medical School, Boston, MA, USA; Center for Genomic Medicine, Massachusetts General Hospital, Boston, MA, USA.

Molecular Metabolism
|May 15, 2020
PubMed
Summary

Exercise training combats cancer cachexia by improving muscle health and lifespan. This study identifies COP9 signalosome complex subunit 2 (COPS2) as a key protein in maintaining muscle function during cancer.

Keywords:
AtrophyCancer cachexiaEndurance exerciseMuscle wastingResponse elements

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Area of Science:

  • Oncology
  • Exercise Physiology
  • Molecular Biology

Background:

  • Cancer cachexia is a debilitating condition characterized by metabolic impairment and muscle wasting.
  • Exercise training is being explored as an adjuvant therapy to mitigate cancer-related side effects.

Purpose of the Study:

  • To investigate the efficacy of exercise training in attenuating cancer cachexia.
  • To elucidate the molecular mechanisms, particularly the role of COP9 signalosome complex subunit 2 (COPS2), underlying exercise's benefits.

Main Methods:

  • In vivo studies using tumor-bearing rats and mice to assess exercise training effects on physical capacity, lifespan, oxidative stress, and muscle function.
  • In vitro experiments with primary myotubes and myoblasts to explore the function of COPS2 in cancer cachexia.
  • Proteomic screening to identify key proteins affected by cancer cachexia and exercise.

Main Results:

  • Exercise training improved running capacity, prolonged lifespan, reduced oxidative stress, and normalized muscle mass and function in tumor-bearing rats.
  • COPS2 was identified as a downregulated protein in skeletal muscle during cancer cachexia, and exercise normalized its expression.
  • COPS2 plays a role in regulating actin cytoskeleton and myotube homeostasis, with its levels correlating with endurance capacity in lung cancer patients.

Conclusions:

  • Exercise training is a promising adjuvant therapy for counteracting cancer cachexia.
  • Novel mechanisms involving COPS2 in regulating myotube homeostasis during cancer cachexia were uncovered, highlighting its therapeutic potential.