ArticleJCI insight2020
Formation of colorectal liver metastases induces musculoskeletal and metabolic abnormalities consistent with exacerbated cachexia.
Article in JCI insight, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 30 citations in OpenAlex.
- Bone Loss, Osteoporosis, and Skeletal Fragility: Hidden Consequences of Cancer Cachexia.Cells · 2026Review
- PEBP4 alleviates muscle wasting in lung cancer cachexia via KEAP1-NRF2-mediated redox homeostasis.Cell death & disease · 2026Article
- Formation of Liver Metastases Is Accompanied by Accelerated Musculoskeletal Deficits in LLC Tumor Hosts.International journal of molecular sciences · 2026Article
- CXCL14 Inhibits Colon Cancer Progression by Modulating Tumor Cell Invasion and Immune Microenvironment.Cells · 2026Article
- Impaired cAMP-PKA-CREB1 signalling drives mitochondrial dysfunction in skeletal muscle during cancer cachexia.Nature metabolism · 2025Article
- Serum miRNA Signatures in Cancer Cachexia Depend on Systemic Inflammation.Current oncology (Toronto, Ont.) · 2025Observational
- Article
- The impact of diet-induced obesity on 5 fluorouracil-induced tumor and liver immune cell cytotoxicity.American journal of physiology. Cell physiology · 2025Article
- Exploring heterogeneity: a dive into preclinical models of cancer cachexia.American journal of physiology. Cell physiology · 2024Review
- The Impact of Non-bone Metastatic Cancer on Musculoskeletal Health.Current osteoporosis reports · 2024Review
- Heterogeneity of weight loss and transcriptomic signatures in pancreatic ductal adenocarcinoma.Journal of cachexia, sarcopenia and muscle · 2024Article
- Mechanisms of Ovarian Cancer-Associated Cachexia.Endocrinology · 2023Review
- Decreased liver B vitamin-related enzymes as a metabolic hallmark of cancer cachexia.Nature communications · 2023Article
- Targeting Mitochondria and Oxidative Stress in Cancer- and Chemotherapy-Induced Muscle Wasting.Antioxidants & redox signaling · 2023Review
- Metastatic or xenograft colorectal cancer models induce divergent anabolic deficits and expression of pro-inflammatory effectors of muscle wasting in a tumor-type-dependent manner.Journal of applied physiology (Bethesda, Md. : 1985) · 2022Article
- Muscle and Bone Defects in Metastatic Disease.Current osteoporosis reports · 2022Review
- RANKL Blockade Reduces Cachexia and Bone Loss Induced by Non-Metastatic Ovarian Cancer in Mice.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2022Article
- The Mitochondria-Targeting Agent MitoQ Improves Muscle Atrophy, Weakness and Oxidative Metabolism in C26 Tumor-Bearing Mice.Frontiers in cell and developmental biology · 2022Article
- Nutrition challenges of cancer cachexia.JPEN. Journal of parenteral and enteral nutrition · 2021Review
- Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 2 countries.
Funding
Abstract
Advanced colorectal cancer (CRC) is often accompanied by development of liver metastases (LMs) and skeletal muscle wasting (i.e., cachexia). Despite plaguing the majority of CRC patients, cachexia remains unresolved. By using mice injected with Colon-26 mouse tumors, either subcutaneously (s.c.; C26) or intrasplenically to mimic hepatic dissemination of cancer cells (mC26), here we aimed to further characterize functional, molecular, and metabolic effects on skeletal muscle and examine whether LMs exacerbate CRC-induced cachexia. C26-derived LMs were associated with progressive loss of body weight, as well as with significant reductions in skeletal muscle size and strength, in line with reduced phosphorylation of markers of protein anabolism and enhanced protein catabolism. mC26 hosts showed prevalence of fibers with glycolytic metabolism and enhanced lipid accumulation, consistent with abnormalities of mitochondrial homeostasis and energy metabolism. In a comparison with mice bearing s.c. C26, cachexia appeared exacerbated in the mC26 hosts, as also supported by differentially expressed pathways within skeletal muscle. Overall, our model recapitulates the cachectic phenotype of metastatic CRC and reveals that formation of LMs resulting from CRC exacerbate cancer-induced skeletal muscle wasting by promoting differential gene expression signatures.
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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.