ArticleMolecular therapy. Nucleic acids2022
Skeletal muscle-specific overexpression of miR-486 limits mammary tumor-induced skeletal muscle functional limitations.
Article in Molecular therapy. Nucleic acids, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 18 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
18 citing papers in PubMed, 18 citations in OpenAlex.
- Circulating MicroRNAs Reflect Body Composition Features in Newly Diagnosed Breast Cancer.International journal of molecular sciences · 2026Article
- Piezo1 Mechanotransduction in Skeletal Muscle: Convergence with Noncoding RNA Regulation in Myogenesis, Regeneration, and Sarcopenia.International journal of molecular sciences · 2026Review
- Circulating muscle- and inflammation-related microRNAs in breast cancer survivorship: associations with subtype, treatment, timing, and age.Molecular biology reports · 2026Article
- Modulation of miRNA networks by exercise in muscular dystrophies: therapeutic insights and future directions.Molecular and cellular biochemistry · 2026Review
- Recombinant ADAMTS‑1 promotes muscle regeneration accompanied by downregulation of Notch signaling.International journal of molecular medicine · 2026Article
- Exercise-responsive microRNA networks and extracellular vesicle-mediated microRNA signaling in breast cancer: linking tumor signaling, systemic crosstalk, and clinical relevance.Frontiers in oncology · 2026Review
- Local Non-Coding Regulatory Elements in Muscular Dystrophies.International journal of molecular sciences · 2025Review
- Engineering Targeted Gene Delivery Systems for Primary Hereditary Skeletal Myopathies: Current Strategies and Future Perspectives.Biomedicines · 2025Review
- microRNA-133a as an indicator of disease progression and treatment response in X-linked myotubular myopathy.Molecular therapy. Nucleic acids · 2025Article
- RNA signaling in skeletal muscle: the central role of microRNAs and exosomal microRNAs.Frontiers in cell and developmental biology · 2025Review
- The miR-6240 target gene Igf2bp3 promotes myoblast fusion by enhancing myomaker mRNA stability.Cellular & molecular biology letters · 2024Article
- Muscle-enriched microRNA-486-mediated regulation of muscular atrophy and exercise.Journal of physiology and biochemistry · 2024Review
- Myogenic microRNAs as Therapeutic Targets for Skeletal Muscle Mass Wasting in Breast Cancer Models.International journal of molecular sciences · 2024Review
- MicroRNA-542-3p targets Pten to inhibit the myoblasts proliferation but suppresses myogenic differentiation independent of targeted Pten.BMC genomics · 2024Article
- Cardioprotective Effects of Exercise: The Role of Irisin and Exosome.Current vascular pharmacology · 2024Review
- A human skeletal muscle stem/myotube model reveals multiple signaling targets of cancer secretome in skeletal muscle.iScience · 2023Article
- Unveiling the functional and evolutionary landscape of RNA editing in chicken using genomics and transcriptomics.Zoological research · 2022Article
- Extracellular vesicle characteristics and microRNA content in cerebral palsy and typically developed individuals at rest and in response to aerobic exercise.Frontiers in physiology · 2022Article
Corrections and comments
- Erratum issued
Authors and funding
7 authors at 4 institutions in 1 country.
Funding
Abstract
miR-486 is a myogenic microRNA, and its reduced skeletal muscle expression is observed in muscular dystrophy. Transgenic overexpression of miR-486 using muscle creatine kinase promoter (MCK-miR-486) partially rescues muscular dystrophy phenotype. We had previously demonstrated reduced circulating and skeletal muscle miR-486 levels with accompanying skeletal muscle defects in mammary tumor models. To determine whether skeletal muscle miR-486 is functionally similar in dystrophies and cancer, we performed functional limitations and biochemical studies of skeletal muscles of MMTV-Neu mice that mimic HER2+ breast cancer and MMTV-PyMT mice that mimic luminal subtype B breast cancer and these mice crossed to MCK-miR-486 mice. miR-486 significantly prevented tumor-induced reduction in muscle contraction force, grip strength, and rotarod performance in MMTV-Neu mice. In this model, miR-486 reversed cancer-induced skeletal muscle changes, including loss of p53, phospho-AKT, and phospho-laminin alpha 2 (LAMA2) and gain of hnRNPA0 and SRSF10 phosphorylation. LAMA2 is a part of the dystrophin-associated glycoprotein complex, and its loss of function causes congenital muscular dystrophy. Complementing these beneficial effects on muscle, miR-486 indirectly reduced tumor growth and improved survival, which is likely due to systemic effects of miR-486 on production of pro-inflammatory cytokines such as IL-6. Thus, similar to dystrophy, miR-486 has the potential to reverse skeletal muscle defects and cancer burden.
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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 Socratic graph.