ArticleMolecular metabolism2020
Exercise training reverses cancer-induced oxidative stress and decrease in muscle COPS2/TRIP15/ALIEN.
Article in Molecular metabolism, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 39 citations in OpenAlex.
- Cardiac defects in spinal muscular atrophy and the role of SMN in cardiomyocyte homeostasis.bioRxiv : the preprint server for biology · 2026Article
- Moderate Aerobic Training Causes Muscle Wasting in a DMBA-Induced Sarcoma Rat Model.International journal of molecular sciences · 2026Article
- Beyond muscle weakness: pathogenesis of sepsis-induced myopathy and its management.Open medicine (Warsaw, Poland) · 2026Review
- Physical Activity, Exerkines, and Their Role in Cancer Cachexia.International journal of molecular sciences · 2025Review
- Cancer Cachexia.Advances in experimental medicine and biology · 2025Review
- Molecular insights of exercise therapy in disease prevention and treatment.Signal transduction and targeted therapy · 2024Review
- Exercise-augmented THSD7B exhibited a positive prognostic implication and tumor-suppressed functionality in pan-cancer.Frontiers in immunology · 2024Article
- Exercise-downregulated CD300E acted as a negative prognostic implication and tumor-promoted role in pan-cancer.Frontiers in immunology · 2024Article
- Skeletal muscle atrophy, regeneration, and dysfunction in heart failure: Impact of exercise training.Journal of sport and health science · 2023Review
- Article
- Nutritional and Exercise Interventions in Cancer-Related Cachexia: An Extensive Narrative Review.International journal of environmental research and public health · 2022Review
- Exercise protocols: The gap between preclinical and clinical exercise oncology studies.Metabolism open · 2022Article
- Physical exercise at the crossroad between muscle wasting and the immune system: implications for lung cancer cachexia.Journal of cachexia, sarcopenia and muscle · 2022Review
- Review
- Muscle metabolic stress determines cancer cachexia severity in mice.Frontiers in physiology · 2022Article
- Article
- Exercise-A Panacea of Metabolic Dysregulation in Cancer: Physiological and Molecular Insights.International journal of molecular sciences · 2021Review
- Exercise as a therapy for cancer-induced muscle wasting.Sports medicine and health science · 2020Review
- The Role of Cullin-RING Ligases in Striated Muscle Development, Function, and Disease.International journal of molecular sciences · 2020Review
Corrections and comments
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Authors and funding
23 authors at 6 institutions in 4 countries.
Funding
Abstract
objectiveWe tested the hypothesis that exercise training would attenuate metabolic impairment in a model of severe cancer cachexia.
methodsWe used multiple in vivo and in vitro methods to explore the mechanisms underlying the beneficial effects induced by exercise training in tumor-bearing rats.
resultsExercise training improved running capacity, prolonged lifespan, reduced oxidative stress, and normalized muscle mass and contractile function in tumor-bearing rats. An unbiased proteomic screening revealed COP9 signalosome complex subunit 2 (COPS2) as one of the most downregulated proteins in skeletal muscle at the early stage of cancer cachexia. Exercise training normalized muscle COPS2 protein expression in tumor-bearing rats and mice. Lung cancer patients with low endurance capacity had low muscle COPS2 protein expression as compared to age-matched control subjects. To test whether decrease in COPS2 protein levels could aggravate or be an intrinsic compensatory mechanism to protect myotubes from cancer effects, we performed experiments in vitro using primary myotubes. COPS2 knockdown in human myotubes affected multiple cellular pathways, including regulation of actin cytoskeleton. Incubation of cancer-conditioned media in mouse myotubes decreased F-actin expression, which was partially restored by COPS2 knockdown. Direct repeat 4 (DR4) response elements have been shown to positively regulate gene expression. COPS2 overexpression decreased the DR4 activity in mouse myoblasts, and COPS2 knockdown inhibited the effects of cancer-conditioned media on DR4 activity.
conclusionsThese studies demonstrated that exercise training may be an important adjuvant therapy to counteract cancer cachexia and uncovered novel mechanisms involving COPS2 to regulate myotube homeostasis in cancer cachexia.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.