ArticleFrontiers in oncology2026
Regulatory mechanisms of mitochondrial function by cancer-derived exosomes in cachexia.
Article in Frontiers in oncology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Cancer Cachexia in Advanced Renal Cell Carcinoma: From Molecular Mechanisms to Prognostic Assessment.International journal of molecular sciences · 2026Review
- Exosome-Mediated Systemic Signaling: Mechanisms, Disease Integration, and Translational Potential.Current issues in molecular biology · 2026Review
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Authors and funding
9 authors.
Funding
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Abstract
Background: Cancer cachexia is a multifactorial syndrome characterized by progressive skeletal muscle wasting and impaired response to conventional nutritional support, affecting up to 80% of advanced cancer patients and contributing to poor prognosis. Excessive fatty acid oxidation and mitochondrial reactive oxygen species (ROS) generation have been implicated in cachexia-associated muscle atrophy, but the underlying mechanisms remain unclear. Methods and results: We investigated the role of cancer cell-derived exosomes in metabolic alterations of skeletal muscle cells. Exosomes from a pro-cachectic renal carcinoma cell line (RXF393) induced myotube atrophy, enhanced mitochondrial ROS production, impaired mitochondrial respiration, and reduced expression of isocitrate dehydrogenase 2 (IDH2) and respiratory chain complex subunits compared to observations in non-cachectic controls. miRNA profiling identified enrichment of miR-1260b in pro-cachectic exosomes, and transfection with a miR-1260b mimic reproduced these phenotypes, including IDH2 downregulation, impaired antioxidant defense, and mitochondrial dysfunction. Conclusion: These findings demonstrate that cancer-derived exosomal miR-1260b suppresses IDH2, disrupts mitochondrial redox balance, and promotes muscle wasting. This study reveals a mechanistic link between exosomal miRNAs and mitochondrial dysfunction in cancer cachexia and suggests that maintaining mitochondrial redox homeostasis may represent a novel therapeutic strategy.
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