ArticleScience advances2023
TWIST2-mediated chromatin remodeling promotes fusion-negative rhabdomyosarcoma.
Article in Science advances, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
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The trial behind it
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Who cites it
12 citing papers in PubMed, 12 citations in OpenAlex.
- Paediatric Therapeutic Development Workshop on rhabdomyosarcoma.British journal of cancer · 2026Review
- Network-based integrative analysis of multi-level regulatory mechanisms associated with glyphosate exposure.Frontiers in bioinformatics · 2026Article
- Unveiling the clinical significance of RNA pseudouridine in colorectal cancer.Science China. Life sciences · 2025Article
- The LncRNA STEAP3-AS1 promotes liver metastasis in colorectal cancer by regulating histone lactylation through chromatin remodelling.Journal of experimental & clinical cancer research : CR · 2025Article
- Shared chromatin remodeling mutations drive concurrent rhabdomyosarcoma and leukemia in a pediatric patient.Discover oncology · 2025Article
- The effects of CypA on apoptosis: potential target for the treatment of diseases.Applied microbiology and biotechnology · 2024Review
- Role of CD73 and the purinergic signaling pathway in the pathogenesis of fusion-negative rhabdomyosarcoma.Purinergic signalling · 2024Article
- CD73 contributes to the pathogenesis of fusion-negative rhabdomyosarcoma through the purinergic signaling pathway.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Contemporary preclinical mouse models for pediatric rhabdomyosarcoma: from bedside to bench to bedside.Frontiers in oncology · 2024Article
- Transcription factor NFYa controls cardiomyocyte metabolism and proliferation during mouse fetal heart development.Developmental cell · 2023Article
- PROTAC-Based Protein Degradation as a Promising Strategy for Targeted Therapy in Sarcomas.International journal of molecular sciences · 2023Review
- Opposing gene regulatory programs governing myofiber development and maturation revealed at single nucleus resolution.Nature communications · 2023Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
Abstract
Rhabdomyosarcoma (RMS) is a common soft tissue sarcoma in children that resembles developing skeletal muscle. Unlike normal muscle cells, RMS cells fail to differentiate despite expression of the myogenic determination protein MYOD. The TWIST2 transcription factor is frequently overexpressed in fusion-negative RMS (FN-RMS). TWIST2 blocks differentiation by inhibiting MYOD activity in myoblasts, but its role in FN-RMS pathogenesis is incompletely understood. Here, we show that knockdown of TWIST2 enables FN-RMS cells to exit the cell cycle and undergo terminal myogenesis. TWIST2 knockdown also substantially reduces tumor growth in a mouse xenograft model of FN-RMS. Mechanistically, TWIST2 controls H3K27 acetylation at distal enhancers by interacting with the chromatin remodelers SMARCA4 and CHD3 to activate growth-related target genes and repress myogenesis-related target genes. These findings provide insights into the role of TWIST2 in maintaining an undifferentiated and tumorigenic state of FN-RMS and highlight the potential of suppressing TWIST2-regulated pathways to treat FN-RMS.
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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.