ArticleNature communications2023
Loss of phosphatase CTDNEP1 potentiates aggressive medulloblastoma by triggering MYC amplification and genomic instability.
Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 28 citations in OpenAlex.
- RNA polymerase II phosphorylation dynamics: from molecular mechanisms to human disease.RNA biology · 2026Review
- Nuclear envelope rupture and resealing: mechanisms, consequences, and disease implications.Biochemical Society transactions · 2026Review
- Protein phosphatase 2A regulates senescence and immunogenicity in medulloblastoma models.The Journal of clinical investigation · 2026Article
- Tumor-derived WNT7A reprograms pulmonary fibroblasts to remodel the metastatic niche and promote bladder cancer lung metastasis.Experimental & molecular medicine · 2026Article
- Hierarchical membrane-chromatin tethering buffers nuclear envelope assembly against alterations in lipid flux.bioRxiv : the preprint server for biology · 2026Article
- The transcription factor LHX2 mediates and enhances oncogenic BMP signaling in medulloblastoma.Cell death and differentiation · 2025Article
- Exploring deep learning and hybrid approaches in molecular subgrouping and prognostic-related genetic signatures of medulloblastoma.Chinese neurosurgical journal · 2025Article
- Deciphering Medulloblastoma: Epigenetic and Metabolic Changes Driving Tumorigenesis and Treatment Outcomes.Biomedicines · 2025Review
- Melanoma antigens in pediatric medulloblastoma contribute to tumor heterogeneity and species-specificity of group 3 tumors.Acta neuropathologica communications · 2025Article
- Suppression of TGF-β/SMAD signaling by an inner nuclear membrane phosphatase complex.Nature communications · 2025Article
- Deletion of 17p in cancers: Guilt by (p53) association.Oncogene · 2025Review
- In-depth inference of transcriptional regulatory networks reveals NPM1 as a therapeutic ribosomal regulator in MYC-amplified medulloblastoma.NPJ precision oncology · 2025Article
- Survival-Related Genes on Chromosomes 6 and 17 in Medulloblastoma.International journal of molecular sciences · 2024Article
- Differential reliance of CTD-nuclear envelope phosphatase 1 on its regulatory subunit in ER lipid synthesis and storage.Molecular biology of the cell · 2024Article
- Structure and mechanism of the human CTDNEP1-NEP1R1 membrane protein phosphatase complex necessary to maintain ER membrane morphology.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- A high-content screen reveals new regulators of nuclear membrane stability.Scientific reports · 2024Article
- Structure and mechanism of the human CTDNEP1-NEP1R1 membrane protein phosphatase complex necessary to maintain ER membrane morphology.bioRxiv : the preprint server for biology · 2023Article
- Beijing Children's Hospital guidelines on the design and conduction of the first standardized database for medulloblastoma.Metabolic brain disease · 2023Article
- A high-content screen reveals new regulators of nuclear membrane stability.bioRxiv : the preprint server for biology · 2023Article
- Research Trends in C-Terminal Domain Nuclear Envelope Phosphatase 1.Life (Basel, Switzerland) · 2023Review
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Authors and funding
25 authors at 6 institutions in 5 countries.
Funding
Abstract
MYC-driven medulloblastomas are highly aggressive childhood brain tumors, however, the molecular and genetic events triggering MYC amplification and malignant transformation remain elusive. Here we report that mutations in CTDNEP1, a CTD nuclear-envelope-phosphatase, are the most significantly enriched recurrent alterations in MYC-driven medulloblastomas, and define high-risk subsets with poorer prognosis. Ctdnep1 ablation promotes the transformation of murine cerebellar progenitors into Myc-amplified medulloblastomas, resembling their human counterparts. CTDNEP1 deficiency stabilizes and activates MYC activity by elevating MYC serine-62 phosphorylation, and triggers chromosomal instability to induce p53 loss and Myc amplifications. Further, phosphoproteomics reveals that CTDNEP1 post-translationally modulates the activities of key regulators for chromosome segregation and mitotic checkpoint regulators including topoisomerase TOP2A and checkpoint kinase CHEK1. Co-targeting MYC and CHEK1 activities synergistically inhibits CTDNEP1-deficient MYC-amplified tumor growth and prolongs animal survival. Together, our studies demonstrate that CTDNEP1 is a tumor suppressor in highly aggressive MYC-driven medulloblastomas by controlling MYC activity and mitotic fidelity, pointing to a CTDNEP1-dependent targetable therapeutic vulnerability.
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