ArticleNature communications2022
The myokine Fibcd1 is an endogenous determinant of myofiber size and mitigates cancer-induced myofiber atrophy.
Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 35 citations in OpenAlex.
- UBA1 knockdown dysregulates UBA1-sensitive proteins and impairs muscle function in models of spinal muscular atrophy X-linked 2.Disease models & mechanisms · 2026Article
- Muscle-Tumor Crosstalk in Exercise Oncology: Exercise-Induced Myokines and Cancer Cachexia.Cancers · 2026Review
- Mechanotransduction Failure and Molecular Rescue in Gastric Cancer: Kinetotherapy Across the IL-6/STAT3-Myostatin/ACVR2B-Akt/mTOR Axis.Medical sciences (Basel, Switzerland) · 2026Review
- Designed Minibinders Rewire Receptor Signaling to Enable Functional Human Myogenic Reprogramming.bioRxiv : the preprint server for biology · 2026Article
- Mechanisms of protein degradation in atrophying muscles: What have we learned during the past decade?The Journal of biological chemistry · 2026Review
- Largely Distinct Post-Translational Modifications Differentiate Skeletal Muscle Wasting Caused by Cancer, Dexamethasone and Aging.Journal of cachexia, sarcopenia and muscle · 2026Article
- Physical Activity, Exerkines, and Their Role in Cancer Cachexia.International journal of molecular sciences · 2025Review
- Musculoskeletal Impairments and Dysfunction in Individuals with Head and Neck Cancer Following Surgery with Neck Dissection-A Systematic Review.Life (Basel, Switzerland) · 2025Review
- The ubiquitin-conjugating enzyme UBE2D maintains a youthful proteome and ensures protein quality control during aging by sustaining proteasome activity.PLoS biology · 2025Article
- A comprehensive review of animal models for cancer cachexia: Implications for translational research.Genes & diseases · 2024Review
- Transgenic sensors reveal compartment-specific effects of aggregation-prone proteins on subcellular proteostasis during aging.Cell reports methods · 2024Article
- Crystal structures of human immune protein FIBCD1 suggest an extended binding site compatible with recognition of pathogen-associated carbohydrate motifs.The Journal of biological chemistry · 2024Article
- AH-6809 mediated regulation of lung adenocarcinoma metastasis through NLRP7 and prognostic analysis of key metastasis-related genes.Frontiers in pharmacology · 2024Article
- Review
- Convergent insulin and TGF-β signalling drives cancer cachexia by promoting aberrant fat body ECM accumulation in a Drosophila tumour model.EMBO reports · 2023Article
- Highlighting the idea of exerkines in the management of cancer patients with cachexia: novel insights and a critical review.BMC cancer · 2023Review
- Platelet-derived chemokines promote skeletal muscle regeneration by guiding neutrophil recruitment to injured muscles.Nature communications · 2023Article
- Modulation of protease expression by the transcription factor Ptx1/PITX regulates protein quality control during aging.Cell reports · 2023Article
- Progressive development of melanoma-induced cachexia differentially impacts organ systems in mice.Cell reports · 2023Article
- Expression of FIBCD1 by intestinal epithelial cells alleviates inflammation-driven tumorigenesis in a mouse model of colorectal cancer.Frontiers in oncology · 2023Article
Corrections and comments
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
Abstract
Decline in skeletal muscle cell size (myofiber atrophy) is a key feature of cancer-induced wasting (cachexia). In particular, atrophy of the diaphragm, the major muscle responsible for breathing, is an important determinant of cancer-associated mortality. However, therapeutic options are limited. Here, we have used Drosophila transgenic screening to identify muscle-secreted factors (myokines) that act as paracrine regulators of myofiber growth. Subsequent testing in mouse myotubes revealed that mouse Fibcd1 is an evolutionary-conserved myokine that preserves myofiber size via ERK signaling. Local administration of recombinant Fibcd1 (rFibcd1) ameliorates cachexia-induced myofiber atrophy in the diaphragm of mice bearing patient-derived melanoma xenografts and LLC carcinomas. Moreover, rFibcd1 impedes cachexia-associated transcriptional changes in the diaphragm. Fibcd1-induced signaling appears to be muscle selective because rFibcd1 increases ERK activity in myotubes but not in several cancer cell lines tested. We propose that rFibcd1 may help reinstate myofiber size in the diaphragm of patients with cancer cachexia.
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