ArticleCancer research2020
MEF2c-Dependent Downregulation of Myocilin Mediates Cancer-Induced Muscle Wasting and Associates with Cachexia in Patients with Cancer.
Article in Cancer research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 52 citations in OpenAlex.
- Skeletal muscle reprogramming of metabolic, ribosomal and developmental pathways contributes to Roux-en-Y gastric bypass-induced adaptation in women.EBioMedicine · 2026Article
- MEF2C: A Novel Transcription Factor Implicated in Human Malignant Tumors.Current topics in medicinal chemistry · 2026Review
- Risk factors for mortality in patients with kidney failure on hemodialysis identified by proteomic analysis of CRIC and PACE studies.Nature communications · 2025Article
- A Comprehensive Bioinformatic Analysis Based on Functional Studies of MEF-2 Family in NSCLC.The Yale journal of biology and medicine · 2025Article
- Cancer-induced FOXP1 disrupts and reprograms skeletal-muscle circadian transcription in cachexia.Cell reports · 2025Article
- Identification of a senescence-associated transcriptional program in skeletal muscle of cachectic pancreatic-tumor-bearing mice.American journal of physiology. Cell physiology · 2025Article
- Local Inflammation Precedes Diaphragm Wasting and Fibrotic Remodelling in a Mouse Model of Pancreatic Cancer.Journal of cachexia, sarcopenia and muscle · 2025Article
- Role of myofiber-specific FoxP1 in pancreatic cancer-induced muscle wasting.American journal of physiology. Cell physiology · 2025Article
- Strategy for drug repurposing in fibroadipogenic replacement during muscle wasting: application to duchenne muscular dystrophy.Frontiers in cell and developmental biology · 2025Article
- Myofiber-specific FoxP1 knockout protects against pancreatic cancer-induced muscle wasting in male but not female mice.bioRxiv : the preprint server for biology · 2024Article
- Exploring heterogeneity: a dive into preclinical models of cancer cachexia.American journal of physiology. Cell physiology · 2024Review
- Defining and Addressing Research Priorities in Cancer Cachexia through Transdisciplinary Collaboration.Cancers · 2024Review
- Jianpi Decoction Combined with Medroxyprogesterone Acetate Alleviates Cancer Cachexia and Prevents Muscle Atrophy by Directly Inhibiting E3 Ubiquitin Ligase.Chinese journal of integrative medicine · 2024Article
- Effects of hibernation on two important contractile tissues in tibetan frogs, Nanorana parkeri: a perspective from transcriptomics and metabolomics approaches.BMC genomics · 2024Article
- Comparative transcriptome analysis of longissimus dorsi muscle reveal potential genes affecting meat trait in Chinese indigenous Xiang pig.Scientific reports · 2024Article
- Optimization of a mouse model of pancreatic cancer to simulate the human phenotypes of metastasis and cachexia.BMC cancer · 2024Article
- Mitochondrial fusion and altered beta-oxidation drive muscle wasting in a Drosophila cachexia model.EMBO reports · 2024Article
- Inflammation-Related Gene ADH1A Regulates the Polarization of Macrophage M1 and Influences the Malignant Progression of Gastric Cancer.Journal of inflammation research · 2024Article
- Myocilin misfolding and glaucoma: A 20-year update.Progress in retinal and eye research · 2023Review
- Blocking muscle wasting via deletion of the muscle-specific E3 ligase MuRF1 impedes pancreatic tumor growth.Communications biology · 2023Article
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Authors and funding
18 authors at 2 institutions in 1 country.
Funding
Abstract
Skeletal muscle wasting is a devastating consequence of cancer that contributes to increased complications and poor survival, but is not well understood at the molecular level. Herein, we investigated the role of Myocilin (Myoc), a skeletal muscle hypertrophy-promoting protein that we showed is downregulated in multiple mouse models of cancer cachexia. Loss of Myoc alone was sufficient to induce phenotypes identified in mouse models of cancer cachexia, including muscle fiber atrophy, sarcolemmal fragility, and impaired muscle regeneration. By 18 months of age, mice deficient in Myoc showed significant skeletal muscle remodeling, characterized by increased fat and collagen deposition compared with wild-type mice, thus also supporting Myoc as a regulator of muscle quality. In cancer cachexia models, maintaining skeletal muscle expression of Myoc significantly attenuated muscle loss, while mice lacking Myoc showed enhanced muscle wasting. Furthermore, we identified the myocyte enhancer factor 2 C (MEF2C) transcription factor as a key upstream activator of Myoc whose gain of function significantly deterred cancer-induced muscle wasting and dysfunction in a preclinical model of pancreatic ductal adenocarcinoma (PDAC). Finally, compared with noncancer control patients, MYOC was significantly reduced in skeletal muscle of patients with PDAC defined as cachectic and correlated with MEF2c. These data therefore identify disruptions in MEF2c-dependent transcription of Myoc as a novel mechanism of cancer-associated muscle wasting that is similarly disrupted in muscle of patients with cachectic cancer. SIGNIFICANCE: This work identifies a novel transcriptional mechanism that mediates skeletal muscle wasting in murine models of cancer cachexia that is disrupted in skeletal muscle of patients with cancer exhibiting cachexia.
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