ArticleProceedings of the National Academy of Sciences of the United States of America2023
A TGF-β/KLF10 signaling axis regulates atrophy-associated genes to induce muscle wasting in pancreatic cancer.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2023. 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.
- Systemic health impact of cancer-associated extracellular vesicles and particles.Nature reviews. Cancer · 2026Review
- Vitamin B3 rescues mitochondrial homeostasis in dexamethasone-induced skeletal muscle atrophy by reducing oxidative stress.Journal of bioenergetics and biomembranes · 2026Article
- Sarcopenia as a Marker of Immunometabolic Vulnerability in Pancreatic Ductal Adenocarcinoma.Cancers · 2026Review
- Mechanisms of protein degradation in atrophying muscles: What have we learned during the past decade?The Journal of biological chemistry · 2026Review
- Signaling networks governing skeletal muscle growth, atrophy, and cachexiaSkeletal muscle · 2025Review
- Comprehensive Identification of the Bovine KLF Gene Family and Its Functional Regulation in Muscle Development: Insights from Single-Nuclei Transcriptomics.Animals : an open access journal from MDPI · 2025Article
- Profibrotic immune cells and fibro-adipogenic progenitors contribute to skeletal muscle extracellular matrix remodeling and fibrosis in cancer cachexia.American journal of physiology. Cell physiology · 2025Article
- Pancreatic Cancer-Derived Extracellular Vesicles Enriched with miR-223-5p Promote Skeletal Muscle Wasting Associated with Cachexia.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Hyperactivation of Transforming Growth Factor-β-Activated Kinase 1 Causes Skeletal Muscle Pathology Reminiscent of Inflammatory Myopathies.The American journal of pathology · 2025Article
- Nutritional Status and Chemotherapy Completion in Resectable Pancreatic Cancer: A Narrative Review.Current oncology (Toronto, Ont.) · 2025Review
- Histidine decarboxylase inhibition attenuates cancer-associated muscle wasting.The Journal of experimental medicine · 2025Article
- Development of a prognostic model for overall survival in neuroblastoma based on Schwann cell-specific genes, clinical predictors, and MYCN amplification.Translational cancer research · 2025Article
- TGFβ1 and RGD Cooperatively Regulate SMAD2/3-Mediated Oncogenic Effects in Prostate Cancer Cells in Bio-Orthogonally Constructed Hydrogels.ACS biomaterials science & engineering · 2025Article
- Single-nucleus transcriptomics reveals subsets of degenerative myonuclei after rotator cuff tear-induced muscle atrophy.Cell proliferation · 2025Article
- The Loss of HJV Aggravates Muscle Atrophy by Promoting the Activation of the TβRII/Smad3 Pathway.International journal of molecular sciences · 2025Article
- KLF12 Aggravates Angiotensin II-Induced Cardiac Remodeling in Male Mice by Transcriptionally Inhibiting SMAD7.Journal of the American Heart Association · 2025Article
- Genetics and biology of pancreatic ductal adenocarcinoma.Genes & development · 2025Review
- Advancing the Understanding and Treatment of Cancer Cachexia: Mechanisms, Therapeutic Approaches, and Future Opportunities.Cancer management and research · 2025Review
- Targeting cancer-induced skeletal damage: a holistic approach to understanding pathophysiology, mechanisms, and management solutions.American journal of cancer research · 2025Review
- Review
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Authors and funding
9 authors.
Funding
Abstract
Cancer cachexia, and its associated complications, represent a large and currently untreatable roadblock to effective cancer management. Many potential therapies have been proposed and tested-including appetite stimulants, targeted cytokine blockers, and nutritional supplementation-yet highly effective therapies are lacking. Innovative approaches to treating cancer cachexia are needed. Members of the Kruppel-like factor (KLF) family play wide-ranging and important roles in the development, maintenance, and metabolism of skeletal muscle. Within the KLF family, we identified KLF10 upregulation in a multitude of wasting contexts-including in pancreatic, lung, and colon cancer mouse models as well as in human patients. We subsequently interrogated loss-of-function of KLF10 as a potential strategy to mitigate cancer associated muscle wasting. In vivo studies leveraging orthotopic implantation of pancreas cancer cells into wild-type and KLF10 KO mice revealed significant preservation of lean mass and robust suppression of pro-atrophy muscle-specific ubiquitin ligases Trim63 and Fbxo32, as well as other factors implicated in atrophy, calcium signaling, and autophagy. Bioinformatics analyses identified Transforming growth factor beta (TGF-β), a known inducer of KLF10 and cachexia promoting factor, as a key upstream regulator of KLF10. We provide direct in vivo evidence that KLF10 KO mice are resistant to the atrophic effects of TGF-β. ChIP-based binding studies demonstrated direct binding to
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