ArticleCell death & disease2018
SNAIL is a key regulator of alveolar rhabdomyosarcoma tumor growth and differentiation through repression of MYF5 and MYOD function.
Article in Cell death & disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed.
- Immune-featured stromal niches associate with response to neoadjuvant immunotherapy in oral squamous cell carcinoma.Cell reports. Medicine · 2025Trial
- Stimulation of Adult Muscle Stem Cells with BMPs Results in Direct Activation of Notch Pathway Genes.Cells · 2026Article
- Clinical characteristics and target exploration via scRNA-seq and high-throughput drug screening of FOXO1 fusion positive rhabdomyosarcoma.Pediatric surgery international · 2025Article
- Molecular Targets in Alveolar Rhabdomyosarcoma: A Narrative Review of Progress and Pitfalls.International journal of molecular sciences · 2025Review
- miR-28: A Tiny Player in Cancer Progression and Other Human Diseases.Biomolecules · 2025Review
- Transforming Growth Factor Beta and Alveolar Rhabdomyosarcoma: A Challenge of Tumor Differentiation and Chemotherapy Response.International journal of molecular sciences · 2024Review
- The Wnt-pathway corepressor TLE3 interacts with the histone methyltransferase KMT1A to inhibit differentiation in Rhabdomyosarcoma.Oncogene · 2024Article
- Co-expression of Twist and Snai1: predictor of poor prognosis and biomarker of treatment resistance in untreated prostate cancer.Molecular biology reports · 2024Article
- Genomic and Epigenetic Changes Drive Aberrant Skeletal Muscle Differentiation in Rhabdomyosarcoma.Cancers · 2023Review
- Impact of AMPK on cervical carcinoma progression and metastasis.Cell death & disease · 2023Article
- Exon skipping in genes encoding lineage-defining myogenic transcription factors in rhabdomyosarcoma.Cold Spring Harbor molecular case studies · 2022Article
- Non-coding RNA in rhabdomyosarcoma progression and metastasis.Frontiers in oncology · 2022Review
- Spontaneous Rupture of Rhabdomyosarcoma of the Testis With Unilateral Ptosis: A Case Report and Literature Review.Frontiers in pediatrics · 2022Article
- Article
- BAF complexes drive proliferation and block myogenic differentiation in fusion-positive rhabdomyosarcoma.Nature communications · 2021Article
- Deciphering the Genomic Landscape and Pharmacological Profile of Uncommon Entities of Adult Rhabdomyosarcomas.International journal of molecular sciences · 2021Article
- Article
- Myogenic Differentiation of iPS Cells Shows Different Efficiency in Simultaneous Comparison of Protocols.Cells · 2021Article
- Enhancement of myogenic differentiation and inhibition of rhabdomyosarcoma progression by miR-28-3p and miR-193a-5p regulated by SNAIL.Molecular therapy. Nucleic acids · 2021Article
- Article
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Rhabdomyosarcoma (RMS) is a mesenchymal tumor of soft tissue in children that originates from a myogenic differentiation defect. Expression of SNAIL transcription factor is elevated in the alveolar subtype of RMS (ARMS), characterized by a low myogenic differentiation status and high aggressiveness. In RMS patients SNAIL level increases with higher stage. Moreover, SNAIL level negatively correlates with MYF5 expression. The differentiation of human ARMS cells diminishes SNAIL level. SNAIL silencing in ARMS cells inhibits proliferation and induces differentiation in vitro, and thereby completely abolishes the growth of human ARMS xenotransplants in vivo. SNAIL silencing induces myogenic differentiation by upregulation of myogenic factors and muscle-specific microRNAs, such as miR-206. SNAIL binds to the MYF5 promoter suppressing its expression. SNAIL displaces MYOD from E-box sequences (CANNTG) that are associated with genes expressed during differentiation and G/C rich in their central dinucleotides. SNAIL silencing allows the re-expression of MYF5 and canonical MYOD binding, promoting ARMS cell myogenic differentiation. In differentiating ARMS cells SNAIL forms repressive complex with histone deacetylates 1 and 2 (HDAC1/2) and regulates their expression. Accordingly, in human myoblasts SNAIL silencing induces differentiation by upregulation of myogenic factors. Our data clearly point to SNAIL as a key regulator of myogenic differentiation and a new promising target for future ARMS therapies.
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