ArticlePloS one2011
The regulation of skeletal muscle protein turnover during the progression of cancer cachexia in the Apc(Min/+) mouse.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 161 papers.
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Who cites it
161 citing papers in PubMed, 252 citations in OpenAlex.
- Longevity of cardiac and skeletal muscle proteins is dependent on tissue and subcellular compartmentation patterns.Cell reports · 2026Article
- Exercise mitigates IL-27-induced muscle atrophy following myocardial infarction through anti-inflammatory mechanisms.Journal of translational medicine · 2026Article
- The relationship between sarcopenia detected in newly diagnosed lung cancer patients and serum levels of IL6, IGF-1 and myostatin.Frontiers in aging · 2026Article
- Skeletal muscle methylome-transcriptome disruptions during the onset and progression of colorectal cancer-induced cachexia.American journal of physiology. Cell physiology · 2026Article
- Reprogramming oncogenic mitochondria in pancreatic adenocarcinoma through BRD4 inhibition leads to programmed cell death.The Journal of pharmacology and experimental therapeutics · 2025Article
- Hyperactivation of Transforming Growth Factor-β-Activated Kinase 1 Causes Skeletal Muscle Pathology Reminiscent of Inflammatory Myopathies.The American journal of pathology · 2025Article
- Early Markers of Cardiac and Skeletal Muscle Metabolic Derangement in the Apc(min/+) Male Mouse.Cancer reports (Hoboken, N.J.) · 2025Article
- Branched-Chain Amino Acids and Di-Alanine Supplementation Attenuates Muscle Atrophy in a Murine Model of Cancer Cachexia.Acta physiologica (Oxford, England) · 2025Article
- Adaptive Proteomic Changes in Protein Metabolism and Mitochondrial Alterations Associated with Resistance to Trastuzumab and Pertuzumab Therapy in HER2-Positive Breast Cancer.International journal of molecular sciences · 2025Article
- Mechanisms and pharmacotherapy of cancer cachexia-associated anorexia.Pharmacology research & perspectives · 2025Review
- Pan-cancer secreted proteome and skeletal muscle regulation: insight from a proteogenomic data-driven knowledge base.Functional & integrative genomics · 2025Review
- Cancer Cachexia.Advances in experimental medicine and biology · 2025Review
- Cancer Cachexia.Advances in experimental medicine and biology · 2025Review
- The Effect of Cachexia on the Feeding Regulation of Skeletal Muscle Protein Synthesis in Tumour-Bearing Mice.Journal of cachexia, sarcopenia and muscle · 2025Article
- Review
- Synergistic power of functional foods and exercise in colorectal cancer control: targeting metabolism, mitochondrial function, redox homeostasis, exercise performance, neuroimmune signaling, and brain-gut axis crosstalk.Frontiers in nutrition · 2025Review
- Transcriptional analysis of cancer cachexia: conserved and unique features across preclinical models and biological sex.American journal of physiology. Cell physiology · 2024Article
- Anabolic deficits and divergent unfolded protein response underlie skeletal and cardiac muscle growth impairments in the Yoshida hepatoma tumor model of cancer cachexia.Physiological reports · 2024Article
- AMPK as a mediator of tissue preservation: time for a shift in dogma?Nature reviews. Endocrinology · 2024Review
- Involvement of the gut microbiota in cancer cachexia.American journal of physiology. Cell physiology · 2024Review
101 more citing papers are in PubMed but not listed here.
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Muscle wasting that occurs with cancer cachexia is caused by an imbalance in the rates of muscle protein synthesis and degradation. The Apc(Min/+) mouse is a model of colorectal cancer that develops cachexia that is dependent on circulating IL-6. However, the IL-6 regulation of muscle protein turnover during the initiation and progression of cachexia in the Apc(Min/+) mouse is not known. Cachexia progression was studied in Apc(Min/+) mice that were either weight stable (WS) or had initial (≤5%), intermediate (6-19%), or extreme (≥20%) body weight loss. The initiation of cachexia reduced %MPS 19% and a further ∼50% with additional weight loss. Muscle IGF-1 mRNA expression and mTOR targets were suppressed with the progression of body weight loss, while muscle AMPK phosphorylation (Thr 172), AMPK activity, and raptor phosphorylation (Ser 792) were not increased with the initiation of weight loss, but were induced as cachexia progressed. ATP dependent protein degradation increased during the initiation and progression of cachexia. However, ATP independent protein degradation was not increased until cachexia had progressed beyond the initial phase. IL-6 receptor antibody administration prevented body weight loss and suppressed muscle protein degradation, without any effect on muscle %MPS or IGF-1 associated signaling. In summary, the %MPS reduction during the initiation of cachexia is associated with IGF-1/mTOR signaling repression, while muscle AMPK activation and activation of ATP independent protein degradation occur later in the progression of cachexia. IL-6 receptor antibody treatment blocked cachexia progression through the suppression of muscle protein degradation, while not rescuing the suppression of muscle protein synthesis. Attenuation of IL-6 signaling was effective in blocking the progression of cachexia, but not sufficient to reverse the process.
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Registered trials
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.