{
  "abstract": "Background: Cachexia is a multifactorial syndrome frequently observed in cancer patients, characterized by progressive weight loss, muscle atrophy, and systemic inflammation. We recently demonstrated that supplementation with FuFA-F2, a naturally occurring lipid found in various foods, increases muscle mass in different metabolic contexts. Here, we investigated whether FuFA-F2 supplementation could prevent tumor-induced muscle wasting and preserve skeletal muscle integrity during cancer cachexia. Methods: In vitro, C2C12 myotubes were exposed to TNF and IFN{gamma} to mimic cachectic conditions, and the effects of FuFA-F2 on myotube morphology were assessed. In vivo, cancer cachexia was induced by subcutaneous injection of C26 adenocarcinoma cells into male CD2F1 mice. Three groups were compared: non-grafted control mice, untreated C26 tumor-bearing mice, and C26 tumor-bearing mice orally supplemented with FuFA-F2 (13 mg/kg/day) for 14 days. Results: In C2C12 myotubes, TNF and IFN{gamma} exposure reduced myotube area by 17% (p < 0.05), whereas FuFA-F2 treatment prevented this atrophy and restored myotube area to control levels (p < 0.05). In vivo, FuFA-F2 supplementation prevented muscle wasting in C26 tumor-bearing mice without affecting tumor growth or the loss of white adipose tissue. After 14 days, hindlimb muscle weight was reduced by 22% in C26 mice compared with controls (0.706 vs. 0.903 g, p < 0.05), whereas muscle weight in FuFA-F2-treated mice (0.835 g) was not significantly different from controls. Consistently, spontaneous wheel activity was markedly reduced in C26 mice during the final four days (-79%; 3.4 vs. 16.5 km, p < 0.05), whereas FuFA-F2-treated mice maintained activity levels closer to those of controls (11.2 km). RNA-seq analysis revealed extensive transcriptional reprogramming of skeletal muscle in response to C26 tumor growth, with 5,465 differentially expressed genes (DEGs; 32% of detected genes) between Control and C26 mice. Notably, FuFA-F2 substantially attenuated this response, with only 366 DEGs (2%) between Control and C26 + FuFA-F2 mice, and principal component analysis (PCA) showed a transcriptomic profile closer to controls. Tumor-induced alterations involved pathways related to proteostasis, inflammation, and tissue remodeling, which were largely prevented or attenuated by FuFA-F2. Consistent with these findings, FuFA-F2 prevented the induction of Myostatin, Activin A, MAFbx and MuRF1, and attenuated muscle fibrosis and local inflammation. Conclusions: These findings demonstrate that FuFA-F2 preserves skeletal muscle mass and function in the C26 model of cancer cachexia, despite ongoing tumor progression. FuFA-F2 markedly attenuates tumor-induced transcriptional reprogramming and associated catabolic, inflammatory and fibrotic responses, supporting its potential as a therapeutic strategy to preserve skeletal muscle during cancer cachexia.",
  "abstract_shown": true,
  "affiliations": [],
  "article_type": "New results",
  "arxiv": null,
  "author_total": 21,
  "authors": [
    {
      "name": "Anaïs Deglos"
    },
    {
      "name": "Jennifer Falconi"
    },
    {
      "name": "Charles Géminard"
    },
    {
      "name": "Christelle Bertrand-Gaday"
    },
    {
      "name": "Béatrice Bonafos"
    },
    {
      "name": "Vanessa Bauer"
    },
    {
      "name": "Lisa Heron-Milhavet"
    },
    {
      "name": "Erwann Durand"
    },
    {
      "name": "Pierre Delobel"
    },
    {
      "name": "Céline Jahannault-Talignani"
    },
    {
      "name": "Cécile Dejoux"
    },
    {
      "name": "Anna Carval"
    },
    {
      "name": "Jatuporn Chaiyut"
    },
    {
      "name": "Laurent Vaysse"
    },
    {
      "name": "Siriluck Liengprayoon"
    },
    {
      "name": "Laurence Pessemesse"
    },
    {
      "name": "Charles Coudray"
    },
    {
      "name": "Walter Vetter"
    },
    {
      "name": "Christine Feillet-Coudray"
    },
    {
      "name": "Alexandre Djiane"
    },
    {
      "name": "François Casas"
    }
  ],
  "bibtex": "https://research.draconitic.com/paper/6wdn1jwd1skfe.bib",
  "cited_by": 0,
  "doi": "10.64898/2026.09.08.750107",
  "fulltext_url": "https://www.biorxiv.org/content/10.64898/2026.09.08.750107v1.full",
  "id": "6wdn1jwd1skfe",
  "issns": [
    "2692-8205"
  ],
  "landing_url": "https://hal.inrae.fr/hal-05802426v1",
  "language": "en",
  "licence": "CC-BY",
  "licence_label": "CC BY",
  "licence_source": "article",
  "licence_url": "https://creativecommons.org/licenses/by/4.0/",
  "metadata_licence": null,
  "native_subjects": [
    [
      "biorxiv",
      "cancer biology"
    ],
    [
      "hal",
      "0.sdv"
    ],
    [
      "openalex",
      "1312|Muscle Physiology and Disorders"
    ]
  ],
  "openalex": "W7212316456",
  "pdf_url": "https://www.biorxiv.org/content/10.64898/2026.09.08.750107v1.full.pdf",
  "pmcid": null,
  "pmid": null,
  "published": "2026-09-08",
  "publisher": "BioRxiv",
  "ris": "https://research.draconitic.com/paper/6wdn1jwd1skfe.ris",
  "sources": [
    {
      "first_seen": "2026-10-30T12:17:58Z",
      "native_id": "hal-05802426",
      "source": "hal",
      "url": "https://hal.inrae.fr/hal-05802426v1"
    },
    {
      "first_seen": "2026-10-30T12:21:10Z",
      "native_id": "10.64898/2026.09.08.750107",
      "source": "biorxiv",
      "url": "https://www.biorxiv.org/content/10.64898/2026.09.08.750107v1"
    }
  ],
  "subjects": [
    {
      "field": "biology",
      "origin": "hal:0.sdv",
      "subfield": "general"
    },
    {
      "field": "medicine",
      "origin": "biorxiv:cancer biology",
      "subfield": "oncology"
    }
  ],
  "title": "Furan fatty acid supplementation protects against muscle atrophy during cancer cachexia",
  "title_text": "Furan fatty acid supplementation protects against muscle atrophy during cancer cachexia",
  "type": "preprint",
  "updated_at": "2026-10-30T12:21:10Z",
  "url": "https://research.draconitic.com/paper/6wdn1jwd1skfe",
  "venue": "BioRxiv",
  "versions": []
}