ArticleCancer research2011
Sequential activation of Snail1 and N-Myc modulates sonic hedgehog-induced transformation of neural cells.
Article in Cancer research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
15 citing papers in PubMed, 22 citations in OpenAlex.
- Silencing IKBKE inhibits the migration and invasion of glioblastoma by promoting Snail1 degradation.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2022Article
- Epithelial-mesenchymal transition transcription factors control pluripotent adult stem cell migrationDevelopment (Cambridge, England) · 2017Article
- EMT- and MET-related processes in nonepithelial tumors: importance for disease progression, prognosis, and therapeutic opportunities.Molecular oncology · 2017Review
- EMT cells increase breast cancer metastasis via paracrine GLI activation in neighbouring tumour cells.Nature communications · 2017Article
- RND3 promotes Snail 1 protein degradation and inhibits glioblastoma cell migration and invasion.Oncotarget · 2016Article
- Delineation of MGMT Hypermethylation as a Biomarker for Veliparib-Mediated Temozolomide-Sensitizing Therapy of Glioblastoma.Journal of the National Cancer Institute · 2016Article
- Review
- Na,K-ATPase β1-subunit is a target of sonic hedgehog signaling and enhances medulloblastoma tumorigenicity.Molecular cancer · 2015Article
- A PTCH1 homolog transcriptionally activated by p53 suppresses Hedgehog signaling.The Journal of biological chemistry · 2014Article
- Targeted treatment for sonic hedgehog-dependent medulloblastoma.Neuro-oncology · 2014Review
- The transcription factor GLI1 interacts with SMAD proteins to modulate transforming growth factor β-induced gene expression in a p300/CREB-binding protein-associated factor (PCAF)-dependent manner.The Journal of biological chemistry · 2014Article
- BET bromodomain inhibition of MYC-amplified medulloblastoma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2014Article
- LIN28A facilitates the transformation of human neural stem cells and promotes glioblastoma tumorigenesis through a pro-invasive genetic program.Oncotarget · 2013Article
- The KDM1A histone demethylase is a promising new target for the epigenetic therapy of medulloblastoma.Acta neuropathologica communications · 2013Article
- The transcription factor GLI1 mediates TGFβ1 driven EMT in hepatocellular carcinoma via a SNAI1-dependent mechanism.PloS one · 2012Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Activation of the Sonic hedgehog (Shh) pathway and increased expression of Gli1 play an important role in proliferation and transformation of granule cell progenitors (GCP) in the developing cerebellum. Medulloblastomas arising from cerebellar GCPs are frequently driven by Shh pathway-activating mutations; however, molecular mechanisms of Shh pathway dysregulation and transformation of neural progenitors remain poorly defined. We report that the transcription factor and oncogene Snail1 (Sna1) is directly induced by Shh pathway activity in GCPs, murine medulloblastomas, and human medulloblastoma cells. Enforced expression of Sna1 was sufficient to induce GCPs and medulloblastoma cell proliferation in the absence of Shh/Gli1 exposure. In addition, enforced expression of Sna1 increased transformation of medulloblastoma cells in vitro and in vivo. Analysis of potential Sna1 targets in neural cells revealed a novel Sna1 target, N-Myc, a transcription factor known to play a role in Shh-mediated GCP proliferation and medulloblastoma formation. We found that Sna1 directly induced transcription of N-Myc in human medulloblastoma cells and that depletion of N-Myc ablated the Sna1-induced proliferation and transformation. Taken together, these results provide further insight into the mechanism of Shh-induced transformation of neural progenitor cells and suggest that induction of Sna1 may serve to amplify the oncogenic potential of Shh pathway activation through N-Myc induction.
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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.