ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2014
Skeletal muscle glycoprotein 130's role in Lewis lung carcinoma-induced cachexia.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 105 papers.
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Who cites it
105 citing papers in PubMed, 142 citations in OpenAlex.
- Circulating granulocyte colony-stimulating factor as a sex-unbiased global marker of lung and colorectal cancer cachexia pre-clinical models.Experimental physiology · 2026Article
- Sepsis-associated skeletal muscle wasting is ameliorated by pharmacological inhibition of the STAT3 signaling pathway in mice.Scientific reports · 2026Article
- Dependence of energy balance and hypothalamic neuropeptide gene expression on initial tumor load in mice.Frontiers in oncology · 2026Article
- Sex impacts inflammatory signaling, body composition, and physical function in tumor-bearing mice receiving chemotherapy.American journal of physiology. Cell physiology · 2026Article
- TAK-242 inhibits toll-like receptor-4 signaling and attenuates cancer-associated muscle atrophy via the p38-C/EBPβ pathway.Journal of molecular histology · 2025Article
- JAK1/2 Inhibition Delays Cachexia and Improves Survival through Increased Food Intake.bioRxiv : the preprint server for biology · 2025Article
- Effect of intrapleural anti-Vascular Endothelial Growth Factor (VEGF) associated with nab paclitaxel in a murine model of malignant pleural effusion.BMC cancer · 2025Article
- Review
- 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
- Unraveling the role of STAT3 in Cancer Cachexia: pathogenic mechanisms and therapeutic opportunities.Frontiers in endocrinology · 2025Review
- Transcriptional analysis of cancer cachexia: conserved and unique features across preclinical models and biological sex.American journal of physiology. Cell physiology · 2024Article
- Exploring heterogeneity: a dive into preclinical models of cancer cachexia.American journal of physiology. Cell physiology · 2024Review
- Females display relatively preserved muscle quality compared with males during the onset and early stages of C26-induced cancer cachexia.Journal of applied physiology (Bethesda, Md. : 1985) · 2023Article
- Adenosine monophosphate-activated protein kinase is elevated in human cachectic muscle and prevents cancer-induced metabolic dysfunction in mice.Journal of cachexia, sarcopenia and muscle · 2023Article
- The time-course of cancer cachexia onset reveals biphasic transcriptional disruptions in female skeletal muscle distinct from males.BMC genomics · 2023Article
- Blocking muscle wasting via deletion of the muscle-specific E3 ligase MuRF1 impedes pancreatic tumor growth.Communications biology · 2023Article
- Article
- Review
- Blocking muscle wasting via deletion of the muscle-specific E3 ubiquitin ligase MuRF1 impedes pancreatic tumor growth.Research square · 2023Article
45 more citing papers are in PubMed but not listed here.
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Authors and funding
4 authors at 1 institution in 1 country.
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Abstract
Chronic inflammation is associated with cachexia-induced skeletal muscle mass loss in cancer. Levels of IL-6 cytokine family members are increased during cancer-related cachexia and induce intracellular signaling through glycoprotein130 (gp130). Although muscle STAT3 and circulating IL-6 are implicated in cancer-induced muscle wasting, there is limited understanding of muscle gp130's role in this process. Therefore, we investigated the role of skeletal muscle gp130 (skm-gp130) in cancer-induced alterations in the regulation of muscle protein turnover. Lewis lung carcinoma (LLC) cells were injected into 8-wk-old skm-gp130-knockout (KO) mice or wild-type mice. Skeletal muscle loss was attenuated by 16% in gp130-KO mice, which coincided with attenuated LLC-induced phosphorylation of muscle STAT3, p38, and FOXO3. gp130 KO did not restore mTOR inhibition or alter AMP-activated protein kinase (AMPK) expression. The induction of atrogin expression and p38 phosphorylation in C2C12 myotubes exposed to LLC-treated medium was attenuated by gp130 inhibition, but mTOR inhibition was not restored. STAT signaling inhibition in LLC-treated myotubes did not attenuate the induction of p38 or AMPK phosphorylation. We concluded that, during LLC-induced cachexia, skm-gp130 regulates muscle mass signaling through STAT3 and p38 for the activation of FOXO3 and atrogin, but does not directly regulate the suppression of mTOR.
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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.