ArticleCell death discovery2022
GDF-15 in tumor-derived exosomes promotes muscle atrophy via Bcl-2/caspase-3 pathway.
Article in Cell death discovery, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
What it found
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Who cites it
54 citing papers in PubMed, 60 citations in OpenAlex.
- Skeletal muscle mass, strength, and physical performance gains are similar between healthy postmenopausal women and postmenopausal breast cancer survivors after 12 weeks of resistance exercise training.Supportive care in cancer : official journal of the Multinational Association of Supportive Care in Cancer · 2024Trial
- Cancer Cell-Derived Small Extracellular Vesicles Are Associated with Impaired C2C12 Myoblast Differentiation.International journal of molecular sciences · 2026Article
- Therapeutic potential of ginseng and ginsenosides on muscle wasting disorders: Cachexia, sarcopenia, anorexia, and aging.Journal of ginseng research · 2026Review
- Epigenetic activation of NK-cell effector programs and caspase-8-dependent apoptosis mediates the antitumor activity of LGP in NSCLC.Journal of ginseng research · 2026Article
- Exosome-Mediated Systemic Signaling: Mechanisms, Disease Integration, and Translational Potential.Current issues in molecular biology · 2026Review
- Systemic Drivers and Molecular Mechanisms of Sarcopenia in Aetiology-Specific End-Stage Liver Disease.Journal of cachexia, sarcopenia and muscle · 2026Observational
- Extracellular vesicles in prostate cancer: current understanding and future perspectives.Journal of the National Cancer Center · 2026Review
- Article
- Research progress on the biological function and molecular mechanism of GDF-15 in solid malignant tumors.World journal of surgical oncology · 2026Review
- Tumor-muscle communication in cancer-associated cachexia (Review).Oncology letters · 2026Review
- C26 and CT26 colorectal cancer models exhibit divergent cachexia phenotypes, intramuscular inflammation, and protein turnover signaling.bioRxiv : the preprint server for biology · 2026Article
- Article
- Separating anorexia -dependent and -independent effects in cancer cachexia.bioRxiv : the preprint server for biology · 2026Article
- The effects of tissue inflammation on cancer cachexia.Biochimica et biophysica acta. Molecular basis of disease · 2026Review
- Human neuromuscular organoids mimic cancer-induced muscle cachexia.Cell reports methods · 2026Article
- Review
- Tumor-derived MG53 aggravates gastrointestinal cancer cachexia related muscle atrophy by inhibiting the TLR4/PI3K/AKT/FOXO3a signaling pathway.Frontiers in oncology · 2026Article
- Extracellular vesicles in cancer-associated cachexia: molecular mechanisms and therapeutic perspectives.Frontiers in cell and developmental biology · 2026Review
- A Citrate Synthase Splice Variant Rewires the TCA Cycle to Promote Colorectal Cancer Progression.Cancer research · 2025Article
- GDF15: An emerging disease target and biomarker of metabolic diseases.Journal of endocrinological investigation · 2025Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Tumor-derived exosomes are emerging mediators of cancer cachexia, a kind of multifactorial syndrome characterized by serious loss of skeletal muscle mass and function. Our previous study had showed that microRNAs in exosomes of C26 colon tumor cells were involved in induction of muscle atrophy. Here, we focus on studying proteins in tumor-derived exosomes which might also contribute to the development of cancer cachexia. Results of comparing the protein profiles of cachexic C26 exosomes and non-cachexic MC38 exosomes suggested that growth differentiation factor 15 (GDF-15) was rich in C26 exosomes. Western blotting analysis confirmed the higher levels of GDF-15 in C26 cells and C26 exosomes, compared with that of MC38 cells. Results of animal study also showed that GDF-15 was rich in tumor tissues, serum exosomes, and gastrocnemius (GA) muscle tissues of C26 tumor-bearing mice. GDF-15 protein could directly induce muscle atrophy of cultured C2C12 myotubes via regulating Bcl-2/caspase-3 pathways. What's more, overexpression of GDF-15 in MC38 cells could increase the potency of MC38 conditioned medium or exosomes in inducing muscle atrophy. Knockdown of GDF-15 in C26 cells decreased the potency of C26 conditioned medium or exosomes in inducing muscle atrophy. These results suggested that GDF-15 in tumor-derived exosomes could contribute to induction of muscle atrophy and also supported the possibility of targeting GDF-15 in treatment of cancer cachexia.
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Registered trials
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.