ArticleOncotarget2015
Sunitinib prevents cachexia and prolongs survival of mice bearing renal cancer by restraining STAT3 and MuRF-1 activation in muscle.
Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 46 citations in OpenAlex.
- Cancer Cachexia in Advanced Renal Cell Carcinoma: From Molecular Mechanisms to Prognostic Assessment.International journal of molecular sciences · 2026Review
- Formation of Liver Metastases Is Accompanied by Accelerated Musculoskeletal Deficits in LLC Tumor Hosts.International journal of molecular sciences · 2026Article
- Multiple organs exhibit exacerbated cachexia in male mice with colon cancer than females.Journal of advanced research · 2026Article
- Early molecular changes predict cancer cachexia in LKB1-deleted mouse models of NSCLC.Clinical and translational medicine · 2025Article
- Comprehensive profiling of chemokine and NETosis-associated genes in sarcopenia: construction of a machine learning-based diagnostic nomogram.Frontiers in medicine · 2025Article
- OBSERVE: guidelines for the refinement of rodent cancer models.Nature protocols · 2024Review
- Cancer cachexia: molecular mechanisms and treatment strategies.Journal of hematology & oncology · 2023Review
- Ginsenoside Rd ameliorates muscle wasting by suppressing the signal transducer and activator of transcription 3 pathway.Journal of cachexia, sarcopenia and muscle · 2022Article
- The p97-Nploc4 ATPase complex plays a role in muscle atrophy during cancer and amyotrophic lateral sclerosis.Journal of cachexia, sarcopenia and muscle · 2022Article
- Sunitinib inhibits STAT3 phosphorylation in cardiac muscle and prevents cardiomyopathy in the mdx mouse model of Duchenne muscular dystrophy.Human molecular genetics · 2022Article
- Article
- Review
- Molecular mechanisms of cancer cachexia‑induced muscle atrophy (Review).Molecular medicine reports · 2020Review
- ACVR2B antagonism as a countermeasure to multi-organ perturbations in metastatic colorectal cancer cachexia.Journal of cachexia, sarcopenia and muscle · 2020Article
- Review
- Article
- Formation of colorectal liver metastases induces musculoskeletal and metabolic abnormalities consistent with exacerbated cachexia.JCI insight · 2020Article
- Muscle alterations in the development and progression of cancer-induced muscle atrophy: a review.Journal of applied physiology (Bethesda, Md. : 1985) · 2020Review
- Musclin, A Myokine Induced by Aerobic Exercise, Retards Muscle Atrophy During Cancer Cachexia in Mice.Cancers · 2019Article
- Inhibition of activin-like kinase 4/5 attenuates cancer cachexia associated muscle wasting.Scientific reports · 2019Article
Corrections and comments
- Commented on by
- Erratum issued
Authors and funding
13 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tyrosine kinase inhibitors, affecting angiogenesis, have shown therapeutic efficacy in renal cell carcinoma (RCC). The increased overall survival is not fully explained by their anti-tumor activity, since these drugs frequently induce disease stabilization rather than regression. RCC patients frequently develop cachectic syndrome. We used the RXF393 human renal carcinoma xenograft that recapitulates the characteristics of the disease, including the growth in the mouse kidney (orthotopic implantation), and the induction of cachexia with subsequent premature death. Sunitinib prevents body weight loss and muscle wasting and significantly improves the survival of RXF393-bearing nude mice. The anti-cachectic effect was not associated to direct anti-tumor activity of the drug. Most relevant is the ability of sunitinib to reverse the cachectic phenotype and rescue the animals from the loss of fat tissue. Body weight loss is prevented also in mice bearing the C26 colon carcinoma, classically reported to induce cachexia in immunocompetent mice. Among the mechanisms, we herein show that sunitinib is able to restrain the overactivation of STAT3 and MuRF-1 pathways, involved in enhanced muscle protein catabolism during cancer cachexia. We suggest that off-target effects of angiogenesis inhibitors targeting STAT3 are worth considering as a therapeutic option for patients who develop cachexia, independently of their anti-tumor activity.
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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.