ArticleCancer research2010
Atoh1 inhibits neuronal differentiation and collaborates with Gli1 to generate medulloblastoma-initiating cells.
Article in Cancer research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers.
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Who cites it
67 citing papers in PubMed, 112 citations in OpenAlex.
- A Conserved Enhancer Locus in Extrachromosomal DNA and Homogeneously Staining Regions Activates MYC Transcription in Group 3 Medulloblastoma.Cancer research · 2026Article
- The SHH/GLI target Netrin-1 supports self-renewal in medulloblastoma tumor cells.Cell communication and signaling : CCS · 2026Article
- Hierarchical regulation of cerebellar neurogenesis by Sin3A-mediated gene repression.bioRxiv : the preprint server for biology · 2025Article
- Genetic modeling of ELP1-associated Sonic hedgehog medulloblastoma identifies MDM2 as a selective therapeutic target.Cancer cell · 2025Article
- Functional characterization of the ATOH1 molecular subtype indicates a pro-metastatic role in small cell lung cancer.Cell reports · 2025Article
- Regulation of primary cilia disassembly through HUWE1-mediated TTBK2 degradation plays a crucial role in cerebellar development and medulloblastoma growth.Cell death and differentiation · 2024Article
- Atoh1 mediated disturbance of neuronal maturation by perinatal hypoxia induces cognitive deficits.Communications biology · 2024Article
- Investigation of YAP-1, OTX-2, and nestin protein expressions in neuroblastoma: a preliminary study.Annals of clinical and translational neurology · 2024Article
- Whole-Genome DNA Methylation Profiling of Intrahepatic Cholangiocarcinoma Reveals Prognostic Subtypes with Distinct Biological Drivers.Cancer research · 2024Article
- Functional Characterisation of the ATOH1 Molecular Subtype Indicates a Pro-Metastatic Role in Small Cell Lung Cancer.bioRxiv : the preprint server for biology · 2024Article
- Phosphorylation of human glioma-associated oncogene 1 on Ser937 regulates Sonic Hedgehog signaling in medulloblastoma.Nature communications · 2024Article
- MYC overexpression and SMARCA4 loss cooperate to drive medulloblastoma formation in mice.Acta neuropathologica communications · 2023Article
- Loss of ATOH1 in Pit Cell Drives Stemness and Progression of Gastric Adenocarcinoma by Activating AKT/mTOR Signaling through GAS1.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- Article
- Multiprotein GLI Transcriptional Complexes as Therapeutic Targets in Cancer.Life (Basel, Switzerland) · 2022Review
- The Tumor Microenvironment of Medulloblastoma: An Intricate Multicellular Network with Therapeutic Potential.Cancers · 2022Review
- Decoding the Roles of Astrocytes and Hedgehog Signaling in Medulloblastoma.Current oncology (Toronto, Ont.) · 2021Review
- Epigenetic regulation in medulloblastoma pathogenesis revealed by genetically engineered mouse models.Cancer science · 2021Review
- Cyclin D1 controls development of cerebellar granule cell progenitors through phosphorylation and stabilization of ATOH1.The EMBO journal · 2021Article
- HIC1 Represses Atoh1 Transcription and Hair Cell Differentiation in the Cochlea.Stem cell reports · 2021Article
7 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
The morphogen and mitogen Sonic Hedgehog (Shh) activates a Gli1-dependent transcription program that drives proliferation of granule neuron progenitors (GNP) within the external germinal layer of the postnatally developing cerebellum. Medulloblastomas with mutations activating the Shh signaling pathway preferentially arise within the external germinal layer, and the tumor cells closely resemble GNPs. Atoh1/Math1, a basic helix-loop-helix transcription factor essential for GNP histogenesis, does not induce medulloblastomas when expressed in primary mouse GNPs that are explanted from the early postnatal cerebellum and transplanted back into the brains of naïve mice. However, enforced expression of Atoh1 in primary GNPs enhances the oncogenicity of cells overexpressing Gli1 by almost three orders of magnitude. Unlike Gli1, Atoh1 cannot support GNP proliferation in the absence of Shh signaling and does not govern expression of canonical cell cycle genes. Instead, Atoh1 maintains GNPs in a Shh-responsive state by regulating genes that trigger neuronal differentiation, including many expressed in response to bone morphogenic protein-4. Therefore, by targeting multiple genes regulating the differentiation state of GNPs, Atoh1 collaborates with the pro-proliferative Gli1-dependent transcriptional program to influence medulloblastoma development.
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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.